• helicobacter pylori
• myocardial infarction
• stroke

• COVID-19
• cervical pathology
• oral pathogens

• Humans
• COVID-19/complications
• SARS-CoV-2
• Coinfection/epidemiology
• Candidiasis, Oral
• Prospective Studies
• Bacteria
• Streptococcus

Helicobacter pylori is usually acquired during childhood. The reports from the last two decades pointed out a decrease in H. pylori prevalence across geographical areas worldwide compared to previously reported data. Most of the studies performed in America found an overall H. pylori infection prevalence of approximately 50%. The most important risk factors in America include being male, poor adherence or difficult access to treatment, and the lack of in-home water service. Despite the descending trend in prevalence worldwide, the overall prevalence in Africa remains very high (70%). Nevertheless, the prevalence of H. pylori in children without gastrointestinal who underwent screening was reported to be only 14.2%. The main risk factors in Africa are having a traditional pit or no toilet, poverty, birth order, source of drinking water, or being a farmer. Asia seems to have the widest variations in terms of H. pylori prevalence. Several risk factors were reported in Asia to be associated with this infection, such as lower income and educational level, house crowding, rural residence, ethnicity, the use of tanks as water supplies, alcohol drinking, active smoking, eating spicy food or raw uncooked vegetables, poor living conditions and sanitation. The overall prevalence of H. pylori infection in European children is almost 25%. Portugal has the highest prevalence of all European countries at 66.2% in children 13 years of age. The risk factors in European individuals consist of living in rural areas, eating unwashed fruits and vegetables, not washing hands after school, low parental education and unemployment, and short education duration. Further studies are required to identify the precise mechanisms involved in the discrepancies of H. pylori prevalence worldwide.

H. pylori is involved in the development of 80% of gastric cancers and 5.5% of all malignant conditions worldwide. Its persistence within the host’s stomach causes chronic inflammation, which is a well-known hallmark of carcinogenesis. A wide range of cytokines was reported to be involved in the initiation and long-term persistence of this local and systemic inflammation. IL-8 was among the first cytokines described to be increased in patients with H. pylori infection. Although, this cytokine was initially identified to exert a chemoattracting effect that represents a trigger for the activation of inflammatory cells within H.-pylori-infected mucosa, more recent studies failed in encountering any association between IL-8 and H. pylori infection. IL-6 is a multifunctional, pleiotropic and multipotent cytokine involved in mediating the interaction between innate and adaptive immunity with a dichotomous role acting as both a proinflammatory and an anti-inflammatory cytokine depending on the signaling pathway. IL-1α functions as a promoter of angiogenesis and vascular endothelial cell proliferation in gastric carcinoma since it is closely related to H.-pylori-induced inflammation in children. IL-1β is an essential trigger and enhancer of inflammation. The association between a low IL-1β level and an increased TNF-α level might be considered a risk factor for peptic ulcer disease in the setting of H. pylori infection. IL-10 downregulates both cytotoxic inflammatory responses and cell-mediated immune responses. H. pylori uses the immunosuppressive role of IL-10 to favor its escape from the host’s immune system. TGFβ is a continuous inflammatory mediator that promotes the adherence of H. pylori to the host’s cells and their subsequent colonization. The role of H.-pylori-induced inflammatory responses in the onset of gastric carcinogenesis seems to represent the missing puzzle piece for designing effective preventive and therapeutic strategies in patients with H.-pylori-associated gastric cancer.

• Chronic gastritis
• Cu/Zn ratio
• Polymorphism
• Selenium
• TRPM5

• Case-Control Studies
• Gastritis/genetics
• Helicobacter pylori
• Humans
• Minerals
• TRPM Cation Channels
• Trace Elements

• Children
• Chronic gastritis
• Helicobacter pylori infection
• Innate immunity
• Systemic inflammation
• TLR9

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COVID-19 patients with pre-existing age-related comorbidities have poor outcomes.

Coronavirus disease 19 (COVID-19) is a pandemic condition caused by the new coronavirus SARS-CoV-2. The typical symptoms are fever, cough, shortness of breath, evolving to a clinical picture of pneumonia and, ultimately, death. Nausea and diarrhea are equally frequent, suggesting viral infection or transmission via the gastrointestinal-enteric system. SARS-CoV-2 infects human cells by using angiotensin converting enzyme 2 (ACE2) as a receptor, which is cleaved by transmembrane proteases during host cells infection, thus reducing its activities. ACE2 is a relevant player in the renin-angiotensin system (RAS), counterbalancing the deleterious effects of angiotensin II. Furthermore, intestinal ACE2 functions as a chaperone for the aminoacid transporter B⁰AT1. It has been suggested that B⁰AT1/ACE2 complex in the intestinal epithelium regulates gut microbiota (GM) composition and function, with important repercussions on local and systemic immune responses against pathogenic agents, namely virus. Notably, productive infection of SARS-CoV-2 in ACE2⁺ mature human enterocytes and patients’ GM dysbiosis was recently demonstrated. This review outlines the evidence linking abnormal ACE2 functions with the poor outcomes (higher disease severity and mortality rate) in COVID-19 patients with pre-existing age-related comorbidities and addresses a possible role for GM dysbiosis. The article culminates with the therapeutics opportunities based on these pathways.

• ACE2
• Age-related diseases
• COVID-19
• Gut microbiota dysbiosis
• Poor outcomes
• SARS-CoV-2

• children
• gastritis
• helicobacter pylori
• neutrophil/lymphocyte ratio

• Adolescent
• Biomarkers/blood
• Case-Control Studies
• Child
• Female
• Gastritis/blood
• Gastritis/immunology
• Gastritis/pathology
• Helicobacter Infections/blood
• Helicobacter Infections/immunology
• Helicobacter Infections/pathology
• Helicobacter pylori
• Humans
• Inflammation/blood
• Inflammation/immunology
• Inflammation/pathology
• Male
• Prospective Studies

Ischemic heart disease (IHD) is clinical manifestation of chronic inflammatory progressive pathological process of atherosclerosis in coronary arteries. IHD is the leading cause of morbidity and mortality in the world. The question is whether it is possible to improve and direct the therapeutic treatment of IHD patients in the treatment of the inflammatory process in the atherosclerotic leasions.

A prospective, comparative, analytica,clinically applicable, open-type study was performed. The study was conducted on 80 subjects with controlled biohumoral markers: troponin, CK, CK MB, BNP; markers of atherogenesis: LDL and homocystein; inflammatory markers: CRP, amyloid, cytokines IL-2, IL-6,TNF-alpha. The experimental group of 38 respondents had in addition to the conventional IHD treatment with: ampicillin (which included organosulfur compounds), cyancobalamin, vitamin B complex (B1, B2 and B6) and folacin. A control group of 42 respondents did not have this additional treatment.

Major adverse cardic events (MACE) such as postinfarctic angina pectoris and repeated infarction, need for surgical interventions of myocardial revascularization, signs of cardiac insufficiency and death were observed during the one-year period. There was no correlation between the IL-2, IL-6 and TNF-alpha, as well as CK, CKMB and troponin and MACE in one-year follow-up. There was a strong positive correlation between MACE and CRP (p = 0,0002) and amyloid (p = 0,0005) as inflamatory markers; a strong positive correlation between MACE and homocysteine as an atherogenic marker (p = 0,0002, and amoderate positive correlation between MACE and BNP (p = 0.0403) as ischemic marker and marker of cardiac insufficiency. The echocardiographically monitored systolic function showed a moderate difference in the groups with average higher values in the experimantal group (p = 0.0282).

The applied treatment exhibited a moderate positive effect on the systolic function of LV and significantly reduced the MACE in the work compared to the control group (p <0.0001), and demonstrated a potential anti-inflammatory effect.

• MACE
• ampicillin
• ischemic heart disease
• marker
• vitamin B complex

• Helicobacter pylori
• inflammation
• peptic disease
• platelet/lymphocyte ratio

• Human cytomegalovirus
• Infection
• Meta-analysis
• Vascular disease

• Helicobacter pylori (HP) infection
• insulin resistance
• prediabetic

• Case-Control Studies
• Cross-Sectional Studies
• Early Diagnosis
• Emergency Service, Hospital
• Female
• Humans
• Leukocyte Count
• Lymphocyte Count
• Lymphocytes
• Male
• Middle Aged
• Neutrophils
• Peptic Ulcer Perforation/blood
• Peptic Ulcer Perforation/mortality
• Peptic Ulcer Perforation/therapy
• Predictive Value of Tests
• Retrospective Studies
• Risk Factors
• Sensitivity and Specificity

• C-reactive protein
• Cohort studies
• Gastrointestinal haemorrhage
• Prognosis

Helicobacter pylori (H. pylori) is a known pathogen implicated in genesis of gastritis, peptic ulcer disease, gastric carcinoma and gastric lymphoma. Beyond the stomach, the organism has also been implicated in the causation of immune thrombocytopenia and iron deficiency anemia. Although an area of active clinical research, the role of this gram negative organism in causation of atherosclerosis and coronary artery disease (CAD) remains enigmatic. CAD is a multifactorial disease which results from the atherosclerosis involving coronary arteries. The major risk factors include age, diabetes mellitus, smoking, hypertension and dyslipidemia. The risk of CAD is believed to increase with chronic inflammation. Various organisms like Chlamydia and Helicobacter have been suspected to have a role in genesis of atherosclerosis via causation of chronic inflammation. This paper focuses on available evidence to ascertain if the role of H. pylori in CAD causation has been proven beyond doubt and if eradication may reduce the risk of CAD or improve outcomes in these patients.

• Extra gastric
• Coronary artery disease
• Helicobacter pylori
• Atherosclerosis
• Inflammation

• Helicobacter pylori
• inflammation
• neutrophil/lymphocyte ratio
• peptic disease

Atherosclerosis is becoming an alarming disease for the existence of healthy human beings in the 21^st century. There are a growing number of agents, either modernized life style generated, competitive work culture related or infection with some bacterial or viral agents, documented every year. These infectious agents do not have proper diagnostics or detection availability in many poor and developing countries. Hence, as active medical researchers, we summarize some aspects of infectious agents and their related mechanisms in this review which may be beneficial for new beginners in this field and update awareness in the field of cardiovascular biology.

• Chlamydia pneumoniae
• Helicobacter pylori
• Cytomegalovirus
• Cytokines
• Diagnostics

• Atherosclerosis/epidemiology
• Atherosclerosis/metabolism
• Atherosclerosis/pathology
• Comorbidity
• Coronary Artery Disease/epidemiology
• Coronary Artery Disease/microbiology
• Coronary Artery Disease/pathology
• Coronary Vessels/microbiology
• Coronary Vessels/pathology
• Female
• Helicobacter Infections/complications
• Helicobacter Infections/epidemiology
• Helicobacter Infections/pathology
• Helicobacter pylori/isolation & purification
• Humans
• Iran/epidemiology
• Male
• Middle Aged
• Plaque, Atherosclerotic/epidemiology
• Plaque, Atherosclerotic/microbiology
• Plaque, Atherosclerotic/pathology
• Seroepidemiologic Studies

• Anemia/microbiology
• Animals
• Disease/etiology
• Helicobacter Infections/etiology
• Helicobacter Infections/microbiology
• Helicobacter pylori/physiology
• Humans
• Purpura, Thrombocytopenic, Idiopathic/etiology
• Purpura, Thrombocytopenic, Idiopathic/microbiology
• Stomach Diseases/etiology
• Stomach Diseases/microbiology

Plasma inflammatory markers have been shown to be predictors for cardiovascular risk, however, there is no study where the levels of plasma circulatory markers have been evaluated in coronary artery disease patients (CAD pts) positive for C. pneumoniae IgA and high sensitive C-reactive protein (hsCRP) which may help in better understanding of disease pathogenesis. A total of 192 patients and 192 controls attending the Cardiology Outpatient Department of Safdarjung Hospital were enrolled. The levels of plasma circulatory inflammatory markers were evaluated by ELISA. The levels of circulatory plasma markers (IL-4, IL-8, IL-13, ICAM-1, and VCAM-1) were significantly higher, whereas, levels of IL-10 and IFN-γ were significantly lower in CAD pts compared to healthy controls. The levels of IL-4, IL-8, and ICAM-1 (P = .007, .015, and .048) were significantly higher, however, IL-10 and IFN-γ were significantly lower (P < .001, < .001) in C. pneumoniae IgA positive CAD pts. The levels of IL-4, IL-8, IL-13, ICAM-1, and VCAM-1 were higher but not significant and levels of IL-10 and IFN-γ were significantly (P < .001, < .001) lower in hsCRP positive CAD pts. Our study suggested that circulatory cytokines, namely, IL-4, IL-8, and adhesive molecules like ICAM-1 were enhanced after infection with C. pneumoniae whereas in contrast to this IL-10 and IFN-λ were lowered. Suggesting the important role of these cytokines in progression of CAD.

• C-Reactive Protein/analysis
• Chlamydophila Infections/blood
• Chlamydophila Infections/complications
• Chlamydophila pneumoniae/immunology
• Coronary Disease/blood
• Coronary Disease/physiopathology
• Disease Progression
• Female
• Humans
• Immunoglobulin A/blood
• Interleukin-2/blood
• Interleukin-6/blood
• Male
• Tumor Necrosis Factor-alpha/blood