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Zhang L, Chi J, Wu H, Xia X, Xu C, Hao H, Liu Z. Extracellular vesicles and endothelial dysfunction in infectious diseases. JOURNAL OF EXTRACELLULAR BIOLOGY 2024; 3:e148. [PMID: 38938849 PMCID: PMC11080793 DOI: 10.1002/jex2.148] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Download PDF] [Figures] [Subscribe] [Scholar Register] [Received: 11/06/2023] [Revised: 02/20/2024] [Accepted: 03/14/2024] [Indexed: 06/29/2024]
Abstract
Cardiovascular diseases (CVDs) remain the leading cause of mortality and morbidity globally. Studies have shown that infections especially bacteraemia and sepsis are associated with increased risks for endothelial dysfunction and related CVDs including atherosclerosis. Extracellular vesicles (EVs) are small, sealed membrane-derived structures that are released into body fluids and blood from cells and/or microbes and are critically involved in a variety of important cell functions and disease development, including intercellular communications, immune responses and inflammation. It is known that EVs-mediated mechanism(s) is important in the development of endothelial dysfunction in infections with a diverse spectrum of microorganisms including Escherichia coli, Candida albicans, SARS-CoV-2 (the virus for COVID-19) and Helicobacter pylori. H. pylori infection is one of the most common infections globally. During H. pylori infection, EVs can carry H. pylori components, such as lipopolysaccharide, cytotoxin-associated gene A, or vacuolating cytotoxin A, and transfer these substances into endothelial cells, triggering inflammatory responses and endothelial dysfunction. This review is to illustrate the important role of EVs in the pathogenesis of infectious diseases, and the development of endothelial dysfunction in infectious diseases especially H. pylori infection, and to discuss the potential mechanisms and clinical implications.
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Affiliation(s)
- Linfang Zhang
- Department of GastroenterologyThe Second Affiliated Hospital of Nanchang UniversityNanchangJiangxiChina
- Center for Precision Medicine and Division of Cardiovascular MedicineDepartment of MedicineUniversity of Missouri School of MedicineColumbiaMissouriUSA
| | - Jingshu Chi
- Center for Precision Medicine and Division of Cardiovascular MedicineDepartment of MedicineUniversity of Missouri School of MedicineColumbiaMissouriUSA
- Department of Gastroenterologythe Third Xiangya HospitalCentral South UniversityChangshaHunanChina
| | - Hao Wu
- Center for Precision Medicine and Division of Cardiovascular MedicineDepartment of MedicineUniversity of Missouri School of MedicineColumbiaMissouriUSA
| | - Xiujuan Xia
- Center for Precision Medicine and Division of Cardiovascular MedicineDepartment of MedicineUniversity of Missouri School of MedicineColumbiaMissouriUSA
| | - Canxia Xu
- Department of Gastroenterologythe Third Xiangya HospitalCentral South UniversityChangshaHunanChina
| | - Hong Hao
- Center for Precision Medicine and Division of Cardiovascular MedicineDepartment of MedicineUniversity of Missouri School of MedicineColumbiaMissouriUSA
| | - Zhenguo Liu
- Center for Precision Medicine and Division of Cardiovascular MedicineDepartment of MedicineUniversity of Missouri School of MedicineColumbiaMissouriUSA
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O'Connor HJ. Forty years of Helicobacter pylori infection and changes in findings at esophagogastroduodenoscopy. Helicobacter 2023; 28:e13026. [PMID: 37818739 DOI: 10.1111/hel.13026] [Citation(s) in RCA: 3] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 07/31/2023] [Revised: 09/24/2023] [Accepted: 09/26/2023] [Indexed: 10/13/2023]
Abstract
BACKGROUND It is 40 years since the discovery of Helicobacter pylori infection. Over that time major changes have occurred in esophagogastroduodenoscopy (EGD) findings. The aim of this review is to describe these changes, and the important role H. pylori infection has played in their evolution. METHODS References were identified through searches of PubMed using the search terms-endoscopy time trends, peptic ulcer disease, gastroesophageal reflux disease, upper gastrointestinal cancer, gastric polyps, H. pylori, eosinophilic gastrointestinal disorders, and celiac disease, from 1970 through December 2021. RESULTS The prevalence of H. pylori infection has fallen and consequently, H. pylori-positive peptic ulcer disease has become rare. Gastroesophageal reflux disease is now the commonest disorder diagnosed at EGD, and Barrett's esophagus has increased in parallel. Cancer of the distal stomach has fallen while esophageal adenocarcinoma and reflux-related cardia cancer have risen. Gastric polyps have changed from hyperplastic and adenomas to sporadic fundic gland polyps. Antimicrobial resistance has made H. pylori infection more difficult to eradicate. Eosinophilic gastrointestinal disorders, particularly eosinophilic esophagitis, have emerged as important new allergic disorders. Celiac disease has changed and increased. CONCLUSIONS EGD findings appear to have changed from features suggesting a H. pylori-positive "phenotype" 40 years ago to a H. pylori-negative "phenotype" today. These changes have major implications for the management of gastrointestinal disorders.
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Affiliation(s)
- Humphrey J O'Connor
- Trinity Academic Gastroenterology Group, Trinity Centre for Health Sciences, The University of Dublin, Tallaght University Hospital, Dublin, Ireland
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Malli C, Pandit L, D’Cunha A, Sudhir A. Helicobacter pylori infection may influence prevalence and disease course in myelin oligodendrocyte glycoprotein antibody associated disorder (MOGAD) similar to MS but not AQP4-IgG associated NMOSD. Front Immunol 2023; 14:1162248. [PMID: 37304259 PMCID: PMC10250711 DOI: 10.3389/fimmu.2023.1162248] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/09/2023] [Accepted: 03/30/2023] [Indexed: 06/13/2023] Open
Abstract
Background Helicobacter pylori (Hp) persists after colonizing the gut in childhood, and potentially regulates host immune system through this process. Earlier studies have shown that Hp infection in childhood, may protect against MS in later life. Such an association was not seen with AQP4-IgG positive NMOSD, while the association with MOGAD is unclear. Objective To evaluate frequency of Hp IgG among patients with MOGAD, MS, NMOSD and matched controls and its effect on disease course. To ascertain whether childhood socio economic factors were linked to prevalence of Hp infection. Methods In all, 99 patients diagnosed to have MOGAD, 99 AQP4 IgG+ NMOSD, 254MS and 243 matched controls were included. Patient demographics, diagnosis, age at disease onset, duration and the last recorded expanded disability status scale (EDSS) were obtained from our records. Socioeconomic and educational status was queried using a previously validated questionnaire. Serum HpIgG was detected using ELISA kits (Vircell, Spain). Result Frequency of Hp IgG was significantly lower among MOGAD (28.3% vs 44%, p-0.007) and MS (21.2% vs 44%, p-0.0001) but not AQP4-IgG+ NMOSD patients (42.4% vs 44%, p-0.78) when compared to controls. Frequency of Hp IgG in MOGAD & MS patients combined (MOGAD-MS) was significantly lower than those with NMOSD (23.2% vs 42.4%, p- 0.0001). Seropositive patients with MOGAD- MS were older (p-0.001. OR -1.04, 95% CI- 1.01- 1.06) and had longer disease duration (p- 0.04, OR- 1.04, 95% CI- 1.002- 1.08) at time of testing. Educational status was lower among parents/caregivers of this study cohort (p- 0.001, OR -2.34, 95% CI- 1.48-3.69) who were Hp IgG+. Conclusions In developing countries Hp infection may be a significant environmental factor related to autoimmune demyelinating CNS disease. Our preliminary data suggests that Hp may exert a differential influence - a largely protective role for MS-MOGAD but not NMOSD and may influence disease onset and course. This differential response maybe related to immuno-pathological similarities between MOGAD and MS in contrast to NMOSD. Our study further underscores the role of Hp as a surrogate marker for poor gut hygiene in childhood and its association with later onset of autoimmune diseases.
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Sia GB, Gestic MA, Utrini MP, Chaim FDM, Chaim EA, Cazzo E. DO HELICOBACTER PYLORI INFECTION AND ERADICATION THERAPY STATUS INFLUENCE WEIGHT LOSS OUTCOMES AND ENDOSCOPIC FINDINGS AFTER ROUX-EN-Y GASTRIC BYPASS?A HISTORICAL COHORT STUDY. ARQUIVOS DE GASTROENTEROLOGIA 2023; 60:57-64. [PMID: 37194781 DOI: 10.1590/s0004-2803.202301000-08] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Subscribe] [Scholar Register] [Received: 08/12/2022] [Accepted: 01/30/2023] [Indexed: 05/18/2023]
Abstract
BACKGROUND Currently, there is conflicting evidence linking Helicobacter pylori (HP) infection with weight loss and endoscopic findings after Roux-en-Y gastric bypass (RYGB). OBJECTIVE To identify correlations between HP infection and its eradication with weight loss and endoscopic findings after RYGB. METHODS This is an observational retrospective cohort study based on a prospectively collected database of individuals who underwent RYGB from 2018-2019 at a tertiary university hospital. HP infection and the HP eradication therapy outcomes were correlated with post-operative weight loss and endoscopic findings. Individuals were classified according to the status of HP infection into four groups: no infection; successful eradication; refractory infection; and new-onset infection. RESULTS Of 65 individuals, 87% were female and the mean age was 39±11.2 years. Body mass index significantly decreased from 36.2±3.6 to 26.7±3.3 kg/m2 one year after RYGB (P<0.0001). The percentage of total weight loss (%TWL) was 25.9±7.2% and the percentage of excess weight loss was 89.4±31.7%. HP infection prevalence decreased from 55.4% to 27.7% (p=0.001); 33.8% never had HP infection, 38.5% were successfully treated, 16.9% had refractory infection and 10.8 % had new-onset HP infection. %TWL was 27.3±7.5% in individuals who never had HP, 25.4±8.1% in the successfully treated, 25.7±5.2% in those with refractory infection, and 23.4±6.4% in the new-onset HP infection group; there were no significant differences among the four groups (P=0.6). Pre-operative HP infection significantly associated with gastritis (P=0.048). New-onset HP infections significantly associated with a lower frequency of jejunal erosions after surgery (P=0.048). CONCLUSION No effects of the HP infection on weight loss were identified in individuals undergoing RYGB. A higher prevalence of gastritis was observed in individuals with HP infection before RYGB. New-onset HP infection after RYGB was a protective factor for jejunal erosions.
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Affiliation(s)
- Gabriela Beatriz Sia
- Universidade Estadual de Campinas, Faculdade de Ciências Médicas, Departamento de Cirurgia, Campinas, SP, Brasil
| | - Martinho Antonio Gestic
- Universidade Estadual de Campinas, Faculdade de Ciências Médicas, Departamento de Cirurgia, Campinas, SP, Brasil
| | - Murillo Pimentel Utrini
- Universidade Estadual de Campinas, Faculdade de Ciências Médicas, Departamento de Cirurgia, Campinas, SP, Brasil
| | - Felipe David Mendonça Chaim
- Universidade Estadual de Campinas, Faculdade de Ciências Médicas, Departamento de Cirurgia, Campinas, SP, Brasil
| | - Elinton Adami Chaim
- Universidade Estadual de Campinas, Faculdade de Ciências Médicas, Departamento de Cirurgia, Campinas, SP, Brasil
| | - Everton Cazzo
- Universidade Estadual de Campinas, Faculdade de Ciências Médicas, Departamento de Cirurgia, Campinas, SP, Brasil
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Arjmandi D, Abdollahi A, Ardekani A, Razavian I, Razavian E, Sartip B, Mahjour S, Parsa H, Kyvanani NA, Marhoommirzabak E, Kountouras J, Rostami A. Helicobacter pylori infection and risk of multiple sclerosis: An updated meta-analysis. Helicobacter 2022; 27:e12927. [PMID: 36046943 DOI: 10.1111/hel.12927] [Citation(s) in RCA: 10] [Impact Index Per Article: 3.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 07/18/2022] [Revised: 08/14/2022] [Accepted: 08/19/2022] [Indexed: 12/09/2022]
Abstract
BACKGROUND There is considerable controversy around the question as to whether Helicobacter pylori (H. pylori) infection has a protective or causative role in the development of multiple sclerosis (MS). This study evaluated published information to assess the association between H. pylori infection and MS. METHODS We conducted a comprehensive systematic review of relevant observational studies in international databases. A random-effects model was used to calculate pooled odds ratio (OR) and 95% confidence interval (CI). I2 statistic was used to assess the between-study heterogeneity. Subgroup and meta-regression analyses were applied to identify the source of heterogeneity. RESULTS In total, 22 studies (25 datasets) were eligible for the meta-analysis: 17 datasets had prevalence data and eight datasets had data on the mean titer of anti-H. pylori IgG. The pooled prevalence of H. pylori was 44.1% (908/2606) in the MS patients and 46.1% (1016/2200) in the controls, indicating a non-significant protective effect of H. pylori on MS (OR, 0.82; 95%CI, 0.58-1.17). In the subgroup analysis, studies that used ELISA yielded a significant protective association (OR, 0.59; 95%CI, 0.46-0.77), while a positive non-significant association (OR, 1.33; 95%CI, 0.83-2.15) was found from studies that used other serological methods; interestingly, a significant positive association (OR, 6.64; 95%CI, 2.40-13.76) was found from studies that used histological methods to detect H. pylori infection. CONCLUSIONS Our findings do not support the hypothesis that H. pylori infection represents a protective factor against the development of MS; however, the results varied depending on the diagnostic method(s). Particularly, a significant positive association was identified when studies introduced results based on histological examination, suggesting that active H. pylori infection might be a risk factor for development of MS. Thus, further studies are needed utilizing accurate diagnostic methods to elucidate the association between active H. pylori infection and MS.
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Affiliation(s)
- Delaram Arjmandi
- Immunoregulation Research Center, Health Research Institute, Babol University of Medical Sciences, Babol, Iran
| | - Ali Abdollahi
- Department of Surgery, Faculty of Medicine, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran
| | - Ali Ardekani
- School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran
| | - Iman Razavian
- Department of Neurosurgery, Functional Neurosurgery Research Center, Shohada Tajrish Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran
| | - Elnaz Razavian
- Department of Neurology, Tehran Medical Sciences Branch, Islamic Azad University, Tehran, Iran
| | - Behnam Sartip
- Department of Internal Medicine, Zanjan University of Medical Sciences, Zanjan, Iran
| | - Sanaz Mahjour
- Department of Psychiatry and Behavioral Sciences, Northwestern Feinberg School of Medicine, Chicago, Illinois, USA
| | - Hamid Parsa
- Department of Neurology, University of Visayas, Gullas College of Medicine, Cebu City, Philippines
| | - Nastaran Azizi Kyvanani
- Independent Researcher in the Field of Microbiology and Infectious Diseases, Erfurt, Germany
| | - Elika Marhoommirzabak
- Department of Neurology, University of Visayas, Gullas College of Medicine, Cebu City, Philippines
| | - Jannis Kountouras
- Second Medical Clinic, School of Medicine, Ippokration Hospital, Aristotle University of Thessaloniki, Thessaloniki, Greece
| | - Ali Rostami
- Infectious Diseases and Tropical Medicine Research Center, Health Research Institute, Babol University of Medical Sciences, Babol, Iran
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Haque S, Raina R, Afroze N, Hussain A, Alsulimani A, Singh V, Mishra BN, Kaul S, Kharwar RN. Microbial dysbiosis and epigenetics modulation in cancer development - A chemopreventive approach. Semin Cancer Biol 2022; 86:666-681. [PMID: 34216789 DOI: 10.1016/j.semcancer.2021.06.024] [Citation(s) in RCA: 11] [Impact Index Per Article: 3.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/23/2021] [Revised: 06/22/2021] [Accepted: 06/25/2021] [Indexed: 01/27/2023]
Abstract
An overwhelming number of research articles have reported a strong relationship of the microbiome with cancer. Microbes have been observed more commonly in the body fluids like urine, stool, mucus of people with cancer compared to the healthy controls. The microbiota is responsible for both progression and suppression activities of various diseases. Thus, to maintain healthy human physiology, host and microbiota relationship should be in a balanced state. Any disturbance in this equilibrium, referred as microbiome dysbiosis becomes a prime cause for the human body to become more prone to immunodeficiency and cancer. It is well established that some of these microbes are the causative agents, whereas others may encourage the formation of tumours, but very little is known about how these microbial communications causing change at gene and epigenome level and trigger as well as encourage the tumour growth. Various studies have reported that microbes in the gut influence DNA methylation, DNA repair and DNA damage. The genes and pathways that are altered by gut microbes are also associated with cancer advancement, predominantly those implicated in cell growth and cell signalling pathways. This study exhaustively reviews the current research advancements in understanding of dysbiosis linked with colon, lung, ovarian, breast cancers and insights into the potential molecular targets of the microbiome promoting carcinogenesis, the epigenetic alterations of various potential targets by altered microbiota, as well as the role of various chemopreventive agents for timely prevention and customized treatment against various types of cancers.
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Affiliation(s)
- Shafiul Haque
- Research and Scientific Studies Unit, College of Nursing and Allied Health Sciences, Jazan University, Jazan, 45142, Saudi Arabia; Bursa Uludağ University Faculty of Medicine, Görükle Campus, 16059, Nilüfer, Bursa, Turkey
| | - Ritu Raina
- School of Life Sciences, Manipal Academy of Higher Education, Dubai, United Arab Emirates
| | - Nazia Afroze
- School of Life Sciences, Manipal Academy of Higher Education, Dubai, United Arab Emirates
| | - Arif Hussain
- School of Life Sciences, Manipal Academy of Higher Education, Dubai, United Arab Emirates.
| | - Ahmad Alsulimani
- Medical Laboratory Technology Department, College of Applied Medical Sciences, Jazan University, Jazan, Saudi Arabia
| | - Vineeta Singh
- Department of Biotechnology, Institute of Engineering and Technology, Dr. A.P.J. Abdul Kalam Technical University, Lucknow, 226021, Uttar Pradesh, India
| | - Bhartendu Nath Mishra
- Department of Biotechnology, Institute of Engineering and Technology, Dr. A.P.J. Abdul Kalam Technical University, Lucknow, 226021, Uttar Pradesh, India
| | - Sanjana Kaul
- School of Biotechnology, University of Jammu, Jammu, 180006, J&K, India
| | - Ravindra Nath Kharwar
- Centre of Advanced Study in Botany, Banaras Hindu University, Varanasi, 221005, India
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Anti-Helicobacter pylori, anti-Inflammatory, and Antioxidant Activities of Trunk Bark of Alstonia boonei (Apocynaceae). BIOMED RESEARCH INTERNATIONAL 2022; 2022:9022135. [PMID: 36158881 PMCID: PMC9499789 DOI: 10.1155/2022/9022135] [Citation(s) in RCA: 4] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Subscribe] [Scholar Register] [Received: 07/18/2022] [Accepted: 08/25/2022] [Indexed: 12/14/2022]
Abstract
An ulcer is an erosion of the gastric mucosa that occurs following an imbalance between the aggression and protective factors and/or an infection with Helicobacter pylori (H. pylori). About 90-100% of duodenal ulcers and 70-80% of gastric ulcers are caused by H. pylori. The objective of this work was to evaluate in vitro the anti-H. pylori activity and then the anti-inflammatory and antioxidant properties of aqueous and methanol extracts of Alstonia boonei. The anti-H. pylori tests (CMI and antiureasic activity) were determined using the agar well diffusion method, the microbroth dilution method, and the measurement of ammonia production by the indophenol method; the anti-inflammatory properties were evaluated by inhibition of proteinases, denaturation of albumin, production of NO by macrophages, cell viability, and hemolysis of red blood cells by heat; then, the antioxidant properties were evaluated by the FRAP method (ferric reducing antioxidant power) and the DPPH (1,1-diphenyl-2-picrylhydrazyl) test. The results show that the best trapping of the DPPH radical was obtained with the methanol extract (EC50 = 8.91 μg/mL) compared to the aqueous extract (EC50 = 19.86 μg/mL). The methanol extract also showed greater iron-reducing activity than the aqueous extract and vitamin C. Furthermore, at the concentration of 200 μg/mL, the methanol extract showed a percentage (96.34%) strains of H. pylori higher than that of the aqueous extract (88.52%). The MIC90 of the methanol extract was lower than that of the aqueous extract. The methanol extract showed a higher percentage inhibition (85%) of urease than the aqueous extract (73%). The methanol extract at a concentration of 1000 μg/mL showed the greatest ability to inhibit proteinase activity, albumin denaturation, and red blood cell hemolysis; on the other hand, maximum cell viability and greater production of nitrite oxide by macrophages were obtained with the aqueous extract. Aqueous and methanol extracts of Alstonia boonei possess anti-H. pylori which would probably be linked to their antioxidant and anti-inflammatory properties.
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Murad H, Rafeeq M, Mosli M, Gari M, Basheikh M. Effect of sequential eradication therapy on serum osteoprotegerin levels in patients with Helicobacter pylori infection and co-existing inflammatory bowel disease. J Int Med Res 2021; 49:3000605211060648. [PMID: 34851775 PMCID: PMC8647270 DOI: 10.1177/03000605211060648] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/15/2022] Open
Abstract
Objective To investigate the effect of sequential Helicobacter pylori
eradication therapy on serum osteoprotegerin levels in patients with
H. pylori infection and co-existing inflammatory bowel
disease (IBD). Methods Three groups of patients were involved in this observational cross-sectional
study: IBD (n = 83), H. pylori infection (HP, n = 68), and
H. pylori infection with co-existing IBD (HP + IBD,
n = 52). These groups were compared with a normal control group (NC,
n = 50). Serum osteoprotegerin, serum bone alkaline phosphatase (BALP), and
fecal calprotectin (FC) levels were measured. Results Serum osteoprotegerin levels were significantly correlated with the simple
endoscopic score for Crohn’s disease and Mayo score for ulcerative colitis.
The receiver operating characteristic analysis of osteoprotegerin revealed
high values for the area under the curve, sensitivity, and specificity.
Discriminant analysis illustrated that osteoprotegerin levels significantly
differentiated patients with IBD from healthy controls. Osteoprotegerin and
FC levels distinguished the IBD and HP + IBD groups from the NC and HP
groups. Conclusions Sequential eradication therapy did not affect serum osteoprotegerin levels in
patients with H. pylori infection and co-existing IBD.
Serum osteoprotegerin elevation might be a marker for IBD development in
patients with past or current H. pylori infection.
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Affiliation(s)
- Hussam Murad
- Department of Pharmacology, Faculty of Medicine, Rabigh, King Abdulaziz University, Jeddah, Saudi Arabia.,Department of Pharmacology, Faculty of Medicine, Ain Shams University, Cairo, Egypt
| | - Misbahuddin Rafeeq
- Department of Pharmacology, Faculty of Medicine, Rabigh, King Abdulaziz University, Jeddah, Saudi Arabia
| | - Mahmoud Mosli
- Department of Medicine, Division of Gastroenterology, Faculty of Medicine, King Abdulaziz University, Jeddah, Saudi Arabia
| | - Mamdouh Gari
- Department of Hematology, Faculty of Applied Medical Sciences, 37848King Abdulaziz University, King Abdulaziz University, Jeddah, Saudi Arabia
| | - Mohammed Basheikh
- Department of Medicine, Faculty of Medicine, King Abdulaziz University, Jeddah, Saudi Arabia
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Alexander SM, Retnakumar RJ, Chouhan D, Devi TNB, Dharmaseelan S, Devadas K, Thapa N, Tamang JP, Lamtha SC, Chattopadhyay S. Helicobacter pylori in Human Stomach: The Inconsistencies in Clinical Outcomes and the Probable Causes. Front Microbiol 2021; 12:713955. [PMID: 34484153 PMCID: PMC8416104 DOI: 10.3389/fmicb.2021.713955] [Citation(s) in RCA: 35] [Impact Index Per Article: 8.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/24/2021] [Accepted: 07/20/2021] [Indexed: 12/11/2022] Open
Abstract
Pathogenic potentials of the gastric pathogen, Helicobacter pylori, have been proposed, evaluated, and confirmed by many laboratories for nearly 4 decades since its serendipitous discovery in 1983 by Barry James Marshall and John Robin Warren. Helicobacter pylori is the first bacterium to be categorized as a definite carcinogen by the International Agency for Research on Cancer (IARC) of the World Health Organization (WHO). Half of the world’s population carries H. pylori, which may be responsible for severe gastric diseases like peptic ulcer and gastric cancer. These two gastric diseases take more than a million lives every year. However, the role of H. pylori as sole pathogen in gastric diseases is heavily debated and remained controversial. It is still not convincingly understood, why most (80–90%) H. pylori infected individuals remain asymptomatic, while some (10–20%) develop such severe gastric diseases. Moreover, several reports indicated that colonization of H. pylori has positive and negative associations with several other gastrointestinal (GI) and non-GI diseases. In this review, we have discussed the state of the art knowledge on “H. pylori factors” and several “other factors,” which have been claimed to have links with severe gastric and duodenal diseases. We conclude that H. pylori infection alone does not satisfy the “necessary and sufficient” condition for developing aggressive clinical outcomes. Rather, the cumulative effect of a number of factors like the virulence proteins of H. pylori, local geography and climate, genetic background and immunity of the host, gastric and intestinal microbiota, and dietary habit and history of medicine usage together determine whether the H. pylori infected person will remain asymptomatic or will develop one of the severe gastric diseases.
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Affiliation(s)
| | | | - Deepak Chouhan
- Rajiv Gandhi Centre for Biotechnology, Trivandrum, India.,Centre for Doctoral Studies, Manipal Academy of Higher Education, Manipal, India
| | | | | | - Krishnadas Devadas
- Department of Gastroenterology, Government Medical College, Trivandrum, India
| | - Namrata Thapa
- Biotech Hub, Department of Zoology, Nar Bahadur Bhandari Degree College, Gangtok, India
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Biofilm Formation as a Complex Result of Virulence and Adaptive Responses of Helicobacter pylori. Pathogens 2020; 9:pathogens9121062. [PMID: 33353223 PMCID: PMC7766044 DOI: 10.3390/pathogens9121062] [Citation(s) in RCA: 49] [Impact Index Per Article: 9.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/27/2020] [Revised: 12/16/2020] [Accepted: 12/17/2020] [Indexed: 12/11/2022] Open
Abstract
Helicobacter pylori is a bacterium that is capable of colonizing a host for many years, often for a lifetime. The survival in the gastric environment is enabled by the production of numerous virulence factors conditioning adhesion to the mucosa surface, acquisition of nutrients, and neutralization of the immune system activity. It is increasingly recognized, however, that the adaptive mechanisms of H. pylori in the stomach may also be linked to the ability of this pathogen to form biofilms. Initially, biofilms produced by H. pylori were strongly associated by scientists with water distribution systems and considered as a survival mechanism outside the host and a source of fecal-oral infections. In the course of the last 20 years, however, this trend has changed and now the most attention is focused on the biomedical aspect of this structure and its potential contribution to the therapeutic difficulties of H. pylori. Taking into account this fact, the aim of the current review is to discuss the phenomenon of H. pylori biofilm formation and present this mechanism as a resultant of the virulence and adaptive responses of H. pylori, including morphological transformation, membrane vesicles secretion, matrix production, efflux pump activity, and intermicrobial communication. These mechanisms will be considered in the context of transcriptomic and proteomic changes in H. pylori biofilms and their modulating effect on the development of this complex structure.
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Robinson K, Atherton JC. The Spectrum of Helicobacter-Mediated Diseases. ANNUAL REVIEW OF PATHOLOGY-MECHANISMS OF DISEASE 2020; 16:123-144. [PMID: 33197219 DOI: 10.1146/annurev-pathol-032520-024949] [Citation(s) in RCA: 73] [Impact Index Per Article: 14.6] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 11/09/2022]
Abstract
Helicobacter pylori is the leading cause of peptic ulcer disease. The infection has been implicated in more than 75% of duodenal ulcer cases and 17% of gastric ulcer cases. H. pylori has been classified as a human carcinogen, since it is the main cause of distal gastric adenocarcinoma and B cell mucosa-associated lymphoid tissue lymphoma. Evidence also links H. pylori with extragastric conditions including iron deficiency anemia, idiopathic thrombocytopenic purpura, and vitamin B12 deficiency. Studies indicate that H. pylori may be protective against other conditions of the gastrointestinal tract (e.g., reflux esophagitis and related pathologies) and elsewhere in the body (e.g., asthma). The infection is asymptomatic in the vast majority of cases; more serious outcomes occur in only 10-15% of infected individuals. Despite extensive research over the past 3 decades, there is no effective vaccine, and the circumstances leading to disease development remain unclear. In addition, there is now a growing prevalence of antimicrobial resistance in H. pylori. This review discusses these important issues.
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Affiliation(s)
- Karen Robinson
- National Institute for Health Research (NIHR) Nottingham Biomedical Research Centre, Nottingham University Hospitals NHS Trust, Nottingham NG7 2UH, United Kingdom.,Nottingham Digestive Diseases Centre, University of Nottingham, Nottingham NG7 2RD United Kingdom;
| | - John C Atherton
- National Institute for Health Research (NIHR) Nottingham Biomedical Research Centre, Nottingham University Hospitals NHS Trust, Nottingham NG7 2UH, United Kingdom.,Nottingham Digestive Diseases Centre, University of Nottingham, Nottingham NG7 2RD United Kingdom;
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Liu XZ, Zhang YM, Jia NY, Zhang H. Helicobacter pylori infection is associated with elevated galactose-deficient IgA1 in IgA nephropathy. Ren Fail 2020; 42:539-546. [PMID: 32524871 PMCID: PMC7946026 DOI: 10.1080/0886022x.2020.1772295] [Citation(s) in RCA: 12] [Impact Index Per Article: 2.4] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/01/2020] [Revised: 05/14/2020] [Accepted: 05/14/2020] [Indexed: 02/07/2023] Open
Abstract
Background: Mucosal immunity plays an important role in the pathogenesis of IgA nephropathy (IgAN). This study aimed to investigate if infection of Helicobacter pylori (H. pylori), a common bacteria in the gastrointestinal tract, associated with IgAN.Methods: This study included 261 patients with IgAN and 46 healthy controls. Clinical information and plasma samples were collected from patients and healthy controls. H. pylori infection was confirmed by western blot. Plasma IgA1 and galactose-deficient IgA1 (Gd-IgA1) levels were detected by specific enzyme-linked immunosorbent assay.Results: Total H. pylori infection rates showed no statistical differences between IgAN patients and healthy controls, but the infection rates of type I H. pylori in IgAN patients were significantly higher than those in healthy controls (44.4 vs. 28.3%, p = 0.040). Compared with uninfected patients, the systolic blood pressure, 24-h proteinuria, and blood urea nitrogen levels were significantly higher in patients with H. pylori infection (126.0 ± 15.5 vs. 119.6 ± 14.5 mmHg, p = 0.010; 1.8 ± 2.7 vs. 1.2 ± 1.4 g/24h, p = 0.013; 7.9 ± 5.4 vs. 6.7 ± 3.9 μmol/L, p = 0.042), especially in patients with type I infection (126.5 ± 15.4 vs. 119.6 ± 14.5 mmHg, p = 0.002; 1.9 ± 2.9 vs. 1.2 ± 1.4 g/24 h, p = 0.033; 8.1 ± 5.6 vs. 6.7 ± 3.9 μmol/L, p = 0.041). Similarly, patients with IgAN and type I H. pylori infection showed higher plasma Gd-IgA1 levels than uninfected patients (5.5 ± 2.2 vs. 4.5 ± 2.2 μg/mL, p = 0.037).Conclusions: Virulent type I H. pylori infection is more common in patients with IgAN. Patients with IgAN and type I H. pylori infection showed lower renal function and higher underglycosylation of plasma IgA1.
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Affiliation(s)
- Xing-Zi Liu
- Renal Division, Peking University First Hospital, Peking University Institute of Nephrology, Beijing, People’s Republic of China
- Key Laboratory of Renal Disease, Ministry of Health of China, Key Laboratory of Chronic Kidney Disease Prevention and Treatment (Peking University), Ministry of Education, Beijing, People’s Republic of China
| | - Yue-Miao Zhang
- Renal Division, Peking University First Hospital, Peking University Institute of Nephrology, Beijing, People’s Republic of China
- Key Laboratory of Renal Disease, Ministry of Health of China, Key Laboratory of Chronic Kidney Disease Prevention and Treatment (Peking University), Ministry of Education, Beijing, People’s Republic of China
| | - Ni-Ya Jia
- Renal Division, Peking University First Hospital, Peking University Institute of Nephrology, Beijing, People’s Republic of China
- Key Laboratory of Renal Disease, Ministry of Health of China, Key Laboratory of Chronic Kidney Disease Prevention and Treatment (Peking University), Ministry of Education, Beijing, People’s Republic of China
| | - Hong Zhang
- Renal Division, Peking University First Hospital, Peking University Institute of Nephrology, Beijing, People’s Republic of China
- Key Laboratory of Renal Disease, Ministry of Health of China, Key Laboratory of Chronic Kidney Disease Prevention and Treatment (Peking University), Ministry of Education, Beijing, People’s Republic of China
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13
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Fisher L, Fisher A, Smith PN. Helicobacter pylori Related Diseases and Osteoporotic Fractures (Narrative Review). J Clin Med 2020; 9:E3253. [PMID: 33053671 PMCID: PMC7600664 DOI: 10.3390/jcm9103253] [Citation(s) in RCA: 7] [Impact Index Per Article: 1.4] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/21/2020] [Revised: 09/28/2020] [Accepted: 10/07/2020] [Indexed: 02/06/2023] Open
Abstract
Osteoporosis (OP) and osteoporotic fractures (OFs) are common multifactorial and heterogenic disorders of increasing incidence. Helicobacter pylori (H.p.) colonizes the stomach approximately in half of the world's population, causes gastroduodenal diseases and is prevalent in numerous extra-digestive diseases known to be associated with OP/OF. The studies regarding relationship between H.p. infection (HPI) and OP/OFs are inconsistent. The current review summarizes the relevant literature on the potential role of HPI in OP, falls and OFs and highlights the reasons for controversies in the publications. In the first section, after a brief overview of HPI biological features, we analyze the studies evaluating the association of HPI and bone status. The second part includes data on the prevalence of OP/OFs in HPI-induced gastroduodenal diseases (peptic ulcer, chronic/atrophic gastritis and cancer) and the effects of acid-suppressive drugs. In the next section, we discuss the possible contribution of HPI-associated extra-digestive diseases and medications to OP/OF, focusing on conditions affecting both bone homeostasis and predisposing to falls. In the last section, we describe clinical implications of accumulated data on HPI as a co-factor of OP/OF and present a feasible five-step algorithm for OP/OF risk assessment and management in regard to HPI, emphasizing the importance of an integrative (but differentiated) holistic approach. Increased awareness about the consequences of HPI linked to OP/OF can aid early detection and management. Further research on the HPI-OP/OF relationship is needed to close current knowledge gaps and improve clinical management of both OP/OF and HPI-related disorders.
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Affiliation(s)
- Leon Fisher
- Department of Gastroenterology, Frankston Hospital, Peninsula Health, Melbourne 3199, Australia
| | - Alexander Fisher
- Department of Geriatric Medicine, The Canberra Hospital, ACT Health, Canberra 2605, Australia;
- Department of Orthopedic Surgery, The Canberra Hospital, ACT Health, Canberra 2605, Australia;
- Australian National University Medical School, Canberra 2605, Australia
| | - Paul N Smith
- Department of Orthopedic Surgery, The Canberra Hospital, ACT Health, Canberra 2605, Australia;
- Australian National University Medical School, Canberra 2605, Australia
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14
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Helicobacter pylori, Peptic Ulcer Disease and Gastric Cancer. GASTROINTESTINAL DISEASES AND THEIR ASSOCIATED INFECTIONS 2019. [DOI: 10.1016/b978-0-323-54843-4.00002-7] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 01/04/2025]
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15
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Whitmire JM, Merrell DS. Helicobacter pylori Genetic Polymorphisms in Gastric Disease Development. ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY 2019; 1149:173-194. [DOI: 10.1007/5584_2019_365] [Citation(s) in RCA: 12] [Impact Index Per Article: 2.0] [Reference Citation Analysis] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 02/07/2023]
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16
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Fernández MF, Reina-Pérez I, Astorga JM, Rodríguez-Carrillo A, Plaza-Díaz J, Fontana L. Breast Cancer and Its Relationship with the Microbiota. INTERNATIONAL JOURNAL OF ENVIRONMENTAL RESEARCH AND PUBLIC HEALTH 2018; 15:1747. [PMID: 30110974 PMCID: PMC6121903 DOI: 10.3390/ijerph15081747] [Citation(s) in RCA: 216] [Impact Index Per Article: 30.9] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Subscribe] [Scholar Register] [Received: 07/06/2018] [Revised: 08/08/2018] [Accepted: 08/11/2018] [Indexed: 02/06/2023]
Abstract
The microorganisms that live symbiotically in human beings are increasingly recognized as important players in health and disease. The largest collection of these microorganisms is found in the gastrointestinal tract. Microbial composition reflects both genetic and lifestyle variables of the host. This microbiota is in a dynamic balance with the host, exerting local and distant effects. Microbial perturbation (dysbiosis) could contribute to the risk of developing health problems. Various bacterial genes capable of producing estrogen-metabolizing enzymes have been identified. Accordingly, gut microbiota is capable of modulating estrogen serum levels. Conversely, estrogen-like compounds may promote the proliferation of certain species of bacteria. Therefore, a crosstalk between microbiota and both endogenous hormones and estrogen-like compounds might synergize to provide protection from disease but also to increase the risk of developing hormone-related diseases. Recent research suggests that the microbiota of women with breast cancer differs from that of healthy women, indicating that certain bacteria may be associated with cancer development and with different responses to therapy. In this review, we discuss recent knowledge about the microbiome and breast cancer, identifying specific characteristics of the human microbiome that may serve to develop novel approaches for risk assessment, prevention and treatment for this disease.
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Affiliation(s)
- Mariana F Fernández
- Department of Radiology, School of Medicine, and Biomedical Research Center, University of Granada, 18071 Granada, Spain.
- Health Research Institute of Granada (ibs.GRANADA), 18010 Granada, Spain.
- Spanish Consortium for Research on Epidemiology and Public Health (CIBERESP), 28029 Madrid, Spain.
| | - Iris Reina-Pérez
- Spanish Consortium for Research on Epidemiology and Public Health (CIBERESP), 28029 Madrid, Spain.
| | - Juan Manuel Astorga
- Department of Radiology, School of Medicine, and Biomedical Research Center, University of Granada, 18071 Granada, Spain.
| | - Andrea Rodríguez-Carrillo
- Department of Radiology, School of Medicine, and Biomedical Research Center, University of Granada, 18071 Granada, Spain.
| | - Julio Plaza-Díaz
- Health Research Institute of Granada (ibs.GRANADA), 18010 Granada, Spain.
- Department of Biochemistry and Molecular Biology II, School of Pharmacy, University of Granada, 18071 Granada, Spain.
- Institute of Nutrition and Food Technology "José Mataix", Biomedical Research Center, Parque Tecnológico Ciencias de la Salud, University of Granada, Armilla, 18100 Granada, Spain.
| | - Luis Fontana
- Health Research Institute of Granada (ibs.GRANADA), 18010 Granada, Spain.
- Department of Biochemistry and Molecular Biology II, School of Pharmacy, University of Granada, 18071 Granada, Spain.
- Institute of Nutrition and Food Technology "José Mataix", Biomedical Research Center, Parque Tecnológico Ciencias de la Salud, University of Granada, Armilla, 18100 Granada, Spain.
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17
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Bravo D, Hoare A, Soto C, Valenzuela MA, Quest AFG. Helicobacter pylori in human health and disease: Mechanisms for local gastric and systemic effects. World J Gastroenterol 2018; 24:3071-3089. [PMID: 30065554 PMCID: PMC6064966 DOI: 10.3748/wjg.v24.i28.3071] [Citation(s) in RCA: 138] [Impact Index Per Article: 19.7] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 04/09/2018] [Revised: 05/17/2018] [Accepted: 06/27/2018] [Indexed: 02/06/2023] Open
Abstract
Helicobacter pylori (H. pylori) is present in roughly 50% of the human population worldwide and infection levels reach over 70% in developing countries. The infection has classically been associated with different gastro-intestinal diseases, but also with extra gastric diseases. Despite such associations, the bacterium frequently persists in the human host without inducing disease, and it has been suggested that H. pylori may also play a beneficial role in health. To understand how H. pylori can produce such diverse effects in the human host, several studies have focused on understanding the local and systemic effects triggered by this bacterium. One of the main mechanisms by which H. pylori is thought to damage the host is by inducing local and systemic inflammation. However, more recently, studies are beginning to focus on the effects of H. pylori and its metabolism on the gastric and intestinal microbiome. The objective of this review is to discuss how H. pylori has co-evolved with humans, how H. pylori presence is associated with positive and negative effects in human health and how inflammation and/or changes in the microbiome are associated with the observed outcomes.
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Affiliation(s)
- Denisse Bravo
- Oral Microbiology Laboratory, Pathology and Oral Medicine Department, Faculty of Dentistry, Universidad de Chile, Santiago 8380492, Chile
| | - Anilei Hoare
- Oral Microbiology Laboratory, Pathology and Oral Medicine Department, Faculty of Dentistry, Universidad de Chile, Santiago 8380492, Chile
| | - Cristopher Soto
- Oral Microbiology Laboratory, Pathology and Oral Medicine Department, Faculty of Dentistry, Universidad de Chile, Santiago 8380492, Chile
| | - Manuel A Valenzuela
- Advanced Center for Chronic Diseases, Institute for Health-Related Research and Innovation, Faculty of Health Sciences, Universidad Central de Chile, Santiago 8380447, Chile
| | - Andrew FG Quest
- Advanced Center for Chronic Diseases, Center for Studies on Exercise, Metabolism and Cancer, Biomedical Science Institute, Faculty of Medicine, Universidad de Chile, Santiago 8380447, Chile
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18
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Karakullukcu A, Tokman HB, Nepesov S, Demirci M, Saribas S, Vehid S, Caliskan R, Taner Z, Cokugras H, Ziver T, Demiryas S, Kocazeybek B. The protective role of Helicobacter pylori neutrophil-activating protein in childhood asthma. Allergol Immunopathol (Madr) 2017; 45:521-527. [PMID: 28579087 DOI: 10.1016/j.aller.2017.01.008] [Citation(s) in RCA: 9] [Impact Index Per Article: 1.1] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/14/2016] [Accepted: 01/24/2017] [Indexed: 02/06/2023]
Abstract
BACKGROUND Helicobacter pylori quantity and HP-NAP gene expression were evaluated in the faeces of healthy and asthmatic children. METHODS H. pylori DNAs and RNAs were isolated from the stool samples of 92 asthmatic children (AC; 3-8 years) and 88 healthy controls (HC). Quantitative PCR was used to determine the quantity of H. pylori and HP-NAP expression relative to the 16S rRNA (reference gene). Gene expression was analysed using the delta delta-Ct method. RESULTS H. pylori DNA was detected in the stool samples of 18 (20.4%) of the 88 HC (p<0.0001, OR=0.79) and none of AC. No meaningful statistical differences were found between individuals with positive and negative family histories for asthma in AC and HC (p>0.05). H. pylori quantity was higher in seven of 18 H. pylori-positive samples, but HP-NAP expression levels were low in four of these seven samples. Based on a multivariate logistic regression analysis of these three variables together, only males displayed a significant difference based on gender differences (p<0.02) and it was determined that, based on the OR value of 0.46 and the 95% CI range of 0.241-0.888, male gender was an independent protective factor in asthma. CONCLUSIONS HP-NAP levels vary to the relative concentrations of bacteria in the stationary or late logarithmic phases. Different napA expression levels may be caused by different endogenous napA gene expression or different environmental conditions.
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Affiliation(s)
- A Karakullukcu
- Istanbul University, Department of Medical Microbiology Cerrahpasa Medical Faculty, Istanbul University, Istanbul, Turkey
| | - H B Tokman
- Istanbul University, Department of Medical Microbiology Cerrahpasa Medical Faculty, Istanbul University, Istanbul, Turkey
| | - S Nepesov
- Department of Pediatric Infectious Diseases, Clinical Immunology and Allergy, Cerrahpasa Medical Faculty, Istanbul University, Istanbul, Turkey
| | - M Demirci
- Istanbul University, Department of Medical Microbiology Cerrahpasa Medical Faculty, Istanbul University, Istanbul, Turkey
| | - S Saribas
- Istanbul University, Department of Medical Microbiology Cerrahpasa Medical Faculty, Istanbul University, Istanbul, Turkey
| | - S Vehid
- Department of Biostatistics, Istanbul University Cerrahpasa Faculty of Medicine, Istanbul University, Istanbul, Turkey
| | - R Caliskan
- Istanbul University, Department of Medical Microbiology Cerrahpasa Medical Faculty, Istanbul University, Istanbul, Turkey
| | - Z Taner
- Istanbul University, Department of Medical Microbiology Cerrahpasa Medical Faculty, Istanbul University, Istanbul, Turkey
| | - H Cokugras
- Department of Pediatric Infectious Diseases, Clinical Immunology and Allergy, Cerrahpasa Medical Faculty, Istanbul University, Istanbul, Turkey
| | - T Ziver
- Eastern Mediterranean University, Faculty of Health Sciences, Nutrition and Dietic Department, Famagusta, North Cyprus, Cyprus
| | - S Demiryas
- Istanbul University, Department of General Surgery, Cerrahpasa Medical Faculty, Istanbul University, Istanbul, Turkey
| | - B Kocazeybek
- Istanbul University, Department of Medical Microbiology Cerrahpasa Medical Faculty, Istanbul University, Istanbul, Turkey.
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19
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The influence of microorganisms in allergic diseases. Allergol Immunopathol (Madr) 2017; 45:519-520. [PMID: 29110881 DOI: 10.1016/j.aller.2017.10.001] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 10/18/2022]
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20
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The Human Stomach in Health and Disease: Infection Strategies by Helicobacter pylori. Curr Top Microbiol Immunol 2017; 400:1-26. [PMID: 28124147 DOI: 10.1007/978-3-319-50520-6_1] [Citation(s) in RCA: 13] [Impact Index Per Article: 1.6] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 02/07/2023]
Abstract
Helicobacter pylori is a bacterial pathogen which commonly colonizes the human gastric mucosa from early childhood and persists throughout life. In the vast majority of cases, the infection is asymptomatic. H. pylori is the leading cause of peptic ulcer disease and gastric cancer, however, and these outcomes occur in 10-15% of those infected. Gastric adenocarcinoma is the third most common cause of cancer-associated death, and peptic ulcer disease is a significant cause of morbidity. Disease risk is related to the interplay of numerous bacterial host and environmental factors, many of which influence chronic inflammation and damage to the gastric mucosa. This chapter summarizes what is known about health and disease in H. pylori infection, and highlights the need for additional research in this area.
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21
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Meta-analysis of association between Helicobacter pylori infection and multiple sclerosis. Neurosci Lett 2016; 620:1-7. [PMID: 27033666 DOI: 10.1016/j.neulet.2016.03.037] [Citation(s) in RCA: 25] [Impact Index Per Article: 2.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/27/2016] [Revised: 03/08/2016] [Accepted: 03/22/2016] [Indexed: 12/12/2022]
Abstract
Despite recent research focus on the association between Helicobacter pylori (H. pylori) infection and multiple sclerosis (MS) there is no consensus about the findings. To obtain a more comprehensive estimate of the association we conducted a meta-analysis to determine the prevalence of H. pylori infection in MS patients and healthy controls. Pubmed and EMBASE were searched to identify eligible studies. Nine studies were selected for inclusion, involving 2806 cases (1553 patients with MS and 1253 controls). Overall, the prevalence of H. pylori infection in MS patients was lower than that in control groups (24.66% vs. 31.84%, OR=0.69, 95% CI: 0.57-0.83, P<0.0001). Subgroup analysis revealed that the levels of H.pylori infection among MS patients were lower than for control subjects in Western countries (11.90% vs. 16.08%, OR=0.63, 95% CI: 0.43-0.91, P=0.01), but were not statistically significant in Eastern countries (39.39% vs. 43.82%, OR=0.79, 95% CI: 0.55-1.14, P=0.20). Our data show that H. pylori infection and MS is negatively correlated, especially in Western countries. Whether H. pylori infection is a protective factor against MS risk should thus be addressed in large-scale and prospective studies.
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22
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Hussain K, Letley DP, Greenaway AB, Kenefeck R, Winter JA, Tomlinson W, Rhead J, Staples E, Kaneko K, Atherton JC, Robinson K. Helicobacter pylori-Mediated Protection from Allergy Is Associated with IL-10-Secreting Peripheral Blood Regulatory T Cells. Front Immunol 2016; 7:71. [PMID: 27014260 PMCID: PMC4779884 DOI: 10.3389/fimmu.2016.00071] [Citation(s) in RCA: 30] [Impact Index Per Article: 3.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/30/2015] [Accepted: 02/15/2016] [Indexed: 12/18/2022] Open
Abstract
Helicobacter pylori infections are usually established in early childhood and continuously stimulate immunity, including T-helper 1 (Th1), Th17, and regulatory T-cell (Treg) responses, throughout life. Although known to be the major cause of peptic ulcer disease and gastric cancer, disease occurs in a minority of those who are infected. Recently, there has been much interest in beneficial effects arising from infection with this pathogen. Published data robustly show that the infection is protective against asthma in mouse models. Epidemiological studies show that H. pylori is inversely associated with human allergy and asthma, but there is a paucity of mechanistic data to explain this. Since Th1 and Treg responses are reported to protect against allergic responses, we investigated if there were links between the human systemic Th1 and Treg response to H. pylori and allergen-specific IgE levels. The human cytokine and T-cell responses were examined using peripheral blood mononuclear cells (PBMCs) from 49 infected and 58 uninfected adult patients. Concentrations of total and allergen-specific plasma IgE were determined by ELISA and ImmunoCAP assays. These responses were analyzed according to major virulence factor genotypes of the patients' colonizing H. pylori strains. An in vitro assay was employed, using PBMCs from infected and uninfected donors, to determine the role of Treg cytokines in the suppression of IgE. Significantly higher frequencies of IL-10-secreting CD4(+)CD25(hi) Tregs, but not H. pylori-specific Th1 cells, were present in the peripheral blood of infected patients. Total and allergen-specific IgE concentrations were lower when there was a strong Treg response, and blocking IL-10 in vitro dramatically restored IgE responses. IgE concentrations were also significantly lower when patients were infected with CagA(+) strains or those expressing the more active i1 form of VacA. The systemic IL-10(+) Treg response is therefore likely to play a role in H. pylori-mediated protection against allergy in humans.
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Affiliation(s)
- Khiyam Hussain
- Nottingham Digestive Diseases Biomedical Research Unit, Queen's Medical Centre, Nottingham University Hospitals, Nottingham, UK; Centre for Biomolecular Sciences, University of Nottingham, Nottingham, UK
| | - Darren P Letley
- Nottingham Digestive Diseases Biomedical Research Unit, Queen's Medical Centre, Nottingham University Hospitals, Nottingham, UK; Centre for Biomolecular Sciences, University of Nottingham, Nottingham, UK
| | - A Borgel Greenaway
- Nottingham Digestive Diseases Biomedical Research Unit, Queen's Medical Centre, Nottingham University Hospitals, Nottingham, UK; Centre for Biomolecular Sciences, University of Nottingham, Nottingham, UK
| | - Rupert Kenefeck
- Nottingham Digestive Diseases Biomedical Research Unit, Queen's Medical Centre, Nottingham University Hospitals, Nottingham, UK; Centre for Biomolecular Sciences, University of Nottingham, Nottingham, UK
| | - Jody A Winter
- Nottingham Digestive Diseases Biomedical Research Unit, Queen's Medical Centre, Nottingham University Hospitals, Nottingham, UK; Centre for Biomolecular Sciences, University of Nottingham, Nottingham, UK
| | - William Tomlinson
- Nottingham Digestive Diseases Biomedical Research Unit, Queen's Medical Centre, Nottingham University Hospitals, Nottingham, UK; Centre for Biomolecular Sciences, University of Nottingham, Nottingham, UK
| | - Joanne Rhead
- Nottingham Digestive Diseases Biomedical Research Unit, Queen's Medical Centre, Nottingham University Hospitals, Nottingham, UK; Centre for Biomolecular Sciences, University of Nottingham, Nottingham, UK
| | - Emily Staples
- Nottingham Digestive Diseases Biomedical Research Unit, Queen's Medical Centre, Nottingham University Hospitals, Nottingham, UK; Centre for Biomolecular Sciences, University of Nottingham, Nottingham, UK
| | - Kazuyo Kaneko
- Nottingham Digestive Diseases Biomedical Research Unit, Queen's Medical Centre, Nottingham University Hospitals, Nottingham, UK; Centre for Biomolecular Sciences, University of Nottingham, Nottingham, UK
| | - John C Atherton
- Nottingham Digestive Diseases Biomedical Research Unit, Queen's Medical Centre, Nottingham University Hospitals, Nottingham, UK; Centre for Biomolecular Sciences, University of Nottingham, Nottingham, UK
| | - Karen Robinson
- Nottingham Digestive Diseases Biomedical Research Unit, Queen's Medical Centre, Nottingham University Hospitals, Nottingham, UK; Centre for Biomolecular Sciences, University of Nottingham, Nottingham, UK
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White JR, Winter JA, Robinson K. Differential inflammatory response to Helicobacter pylori infection: etiology and clinical outcomes. J Inflamm Res 2015; 8:137-47. [PMID: 26316793 PMCID: PMC4540215 DOI: 10.2147/jir.s64888] [Citation(s) in RCA: 50] [Impact Index Per Article: 5.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/16/2022] Open
Abstract
The bacterial pathogen Helicobacter pylori commonly colonizes the human gastric mucosa during early childhood and persists throughout life. The organism has evolved multiple mechanisms for evading clearance by the immune system and, despite inducing inflammation in the stomach, the majority of infections are asymptomatic. H. pylori is the leading cause of peptic ulcer disease and gastric cancer. However, disease outcomes are related to the pattern and severity of chronic inflammation in the gastric mucosa, which in turn is influenced by both bacterial and host factors. Despite over 2 decades of intensive research, there remains an incomplete understanding of the circumstances leading to disease development, due to the fascinating complexity of the host-pathogen interactions. There is accumulating data concerning the virulence factors associated with increased risk of disease, and the majority of these have pro-inflammatory activities. Despite this, only a small proportion of those infected with virulent strains develop disease. Several H. pylori virulence factors have multiple effects on different cell types, including the induction of pro- and anti-inflammatory, immune stimulatory, and immune modulatory responses. The expression of multiple virulence factors is also often linked, making it difficult to assess the meaning of their effects in isolation. Overall, H. pylori is thought to usually modulate inflammation and limit acute damage to the mucosa, enabling the bacteria to persist. If this delicate balance is disturbed, disease may then develop.
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Affiliation(s)
- Jonathan Richard White
- NIHR Biomedical Research Unit in Gastrointestinal and Liver Diseases at Nottingham University Hospitals NHS Trust and The University of Nottingham, Nottingham, UK
| | - Jody Anne Winter
- Interdisciplinary Biomedical Research Centre, School of Science and Technology, Nottingham Trent University, Nottingham, UK
| | - Karen Robinson
- NIHR Biomedical Research Unit in Gastrointestinal and Liver Diseases at Nottingham University Hospitals NHS Trust and The University of Nottingham, Nottingham, UK
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