• Co-occurance
• Gut microbiome
• Irritable bowel syndrome
• Small intestinal bacterial overgrowth

• Humans
• Irritable Bowel Syndrome/microbiology
• Female
• Feces/microbiology
• Male
• Adult
• Gastrointestinal Microbiome
• Middle Aged
• Case-Control Studies
• Intestine, Small/microbiology
• Abdominal Pain/microbiology
• Diarrhea/microbiology
• Blind Loop Syndrome/microbiology
• Blind Loop Syndrome/metabolism
• Surveys and Questionnaires
• Constipation/microbiology

• gut microbiota
• intestinal immunity
• intestinal mucosa
• irritable bowel syndrome

• Humans
• Irritable Bowel Syndrome
• Gastrointestinal Microbiome/physiology
• Intestines
• Intestinal Mucosa
• Immunity, Mucosal

• 81973598 National Natural Science Foundation of China
• 82074214 National Natural Science Foundation of China

• Gut microbiome
• Infectious gastroenteritis
• Inflammation
• Irritable bowel syndrome
• Pathophysiology
• Post infection syndrome

• Animals
• Irritable Bowel Syndrome/diagnosis
• Gastrointestinal Microbiome
• Gastroenteritis/complications
• Communicable Diseases
• Post-Infectious Disorders

• Case-control study
• Environmental chemicals
• Irritable bowel syndrome
• Pesticides

• Humans
• Irritable Bowel Syndrome/epidemiology
• Pesticides
• Case-Control Studies
• Celiac Disease/epidemiology
• Environmental Exposure

• Enterochromaffin cells
• Gastrointestinal microbiome
• Gastroparesis
• Gut barrier dysfunction
• Irritable bowel syndrome

Irritable bowel syndrome (IBS) is a functional gastrointestinal disorder in which recurrent abdominal pain is associated with defecation or a change in bowel habits (constipation, diarrhea, or both), and it is often accompanied by symptoms of abdominal bloating and distension. IBS is an important health care issue because it negatively affects the quality of life of patients and places a considerable financial burden on health care systems. Despite extensive research, the etiology and underlying pathophysiology of IBS remain incompletely understood. Proposed mechanisms involved in its pathogenesis include increased intestinal permeability, changes in the immune system, visceral hypersensitivity, impaired gut motility, and emotional disorders. Recently, accumulating evidence has highlighted the important role of the gut microbiota in the development of IBS. Microbial dysbiosis within the gut is thought to contribute to all aspects of its multifactorial pathogenesis. The last few decades have also seen an increasing interest in the impact of antibiotics on the gut microbiota. Moreover, antibiotics have been suggested to play a role in the development of IBS. Extensive research has established that antibacterial therapy induces remarkable shifts in the bacterial community composition that are quite similar to those observed in IBS. This suggestion is further supported by data from cohort and case-control studies, indicating that antibiotic treatment is associated with an increased risk of IBS. This paper summarizes the main findings on this issue and contributes to a deeper understanding of the link between antibiotic use and the development of IBS.

• Gut microbiota
• Irritable bowel syndrome
• Antibiotics
• Intestinal barrier
• Gut motility
• Gut sensitivity

• Anti-Bacterial Agents/adverse effects
• Dysbiosis/etiology
• Dysbiosis/microbiology
• Dysbiosis/physiopathology
• Gastrointestinal Microbiome/physiology
• Humans
• Irritable Bowel Syndrome/etiology
• Irritable Bowel Syndrome/microbiology
• Irritable Bowel Syndrome/physiopathology
• Quality of Life

• 5-HT
• NLRs
• PRRs
• TLRs
• microorganisms
• serotonin
• tryptophan

• Animals
• Brain-Gut Axis/physiology
• Gastrointestinal Microbiome/physiology
• Humans
• Intestines/metabolism
• Serotonergic Neurons/physiology
• Serotonin/physiology

• Bacteria
• Barrier function
• Diarrhea
• Gut-brain axis
• Infectious gastroenteritis
• Inflammation
• Microbiome

• Animals
• Female
• Gastrointestinal Microbiome
• Humans
• Infections
• Irritable Bowel Syndrome/etiology

• K23 DK103911 NIDDK NIH HHS
• R03 DK120745 NIDDK NIH HHS

• expression analysis
• laser-capture microdissection
• leaky gut
• mast cells
• occludin
• postinfectious functional GI disorders
• tight junctions
• tryptase

• Appetite regulation
• Digestive disease
• Enteroendocrine
• Obesity

Persisting low-grade inflammation is suggested to play a role in postinfectious functional gastrointestinal disorders (PI-FGIDs). The present study examined alterations in duodenal mucosal lymphocytes during and after Giardia gastroenteritis in patients who did, or did not, develop PI-FGIDs.

Duodenal mucosal intraepithelial lymphocytes (IELs) and lamina propria CD3, CD4, CD8, and CD20 lymphocytes were quantified in 28 patients with chronic giardiasis (CG), 66 patients with persistent abdominal symptoms after acute Giardia infection (PI-FGID), 19 recovered controls (RCs), and 16 healthy volunteers (HCs). Associations with illness duration, abdominal symptoms, and histology grade were assessed.

Duodenal CD4 IELs were significantly elevated in CG, then decreased, followed by an upward trend after 1 year in both the PI-FGID and RC groups. Duodenal lamina propria crypt CD4 T cells were decreased in CG, and stayed low for about 14 months before normalizing in both the PI-FGID and RC groups. Lamina propria CD20 cells were persistently elevated in all 3 Giardia-exposed groups. Biopsies with microscopic inflammation showed increased lamina propria CD20 levels.

Duodenal mucosal lymphocyte alterations were prolonged after Giardia infection, but similar in patients who developed PI-FGID and recovered asymptomatic controls.

• Giardia
• B cell
• PI-IBS
• duodenal
• functional gastrointestinal disorders
• histology
• mucosa

• Early-life stress
• Enterochromaffin cell
• Hyperplasia
• Infection
• Inflammation

The Irritable bowel syndrome (IBS) is a functional disorder of alimentary system, which may be caused by infectious gastroenteritis determined as post infectious irritable bowel syndrome (PI-IBS). The prevalence of PI-IBS is reported to be 4-36% in patients with infectious gastroenteritis. The exact mechanism leading to PI-IBS is not fully understood and some factors pertaining to infectious agent and host response may have a role. Rome IV diagnostic criteria provided new definition for PI-IBS. Though it is now considered a well-defined functional disorder of gastrointestinal system, no specific treatment is yet available for PI-IBS. This article reviews the latest issues on these heading about PI-IBS.

• Infectious gastroenteritis
• Irritable Bowel Syndrome
• Prevalence

• Barrier Function
• Campylobacter
• Gastrointestinal Infection
• Microbiome
• Serotonin

• Algorithms
• Animals
• Clinical Decision-Making
• Communicable Diseases/diagnosis
• Communicable Diseases/epidemiology
• Communicable Diseases/therapy
• Consensus
• Delphi Technique
• Gastroenteritis/diagnosis
• Gastroenteritis/epidemiology
• Gastroenteritis/therapy
• Humans
• Irritable Bowel Syndrome/diagnosis
• Irritable Bowel Syndrome/etiology
• Irritable Bowel Syndrome/therapy
• Predictive Value of Tests
• Prevalence
• Prognosis
• Risk Factors

• K23 DK103911 NIDDK NIH HHS

• bacterial infection disease
• clinical microbiology
• irritable bowel syndrome
• parasites
• viruses

Irritable bowel syndrome (IBS) is a common functional gastrointestinal disorder whose treatment is unsatisfactory as its pathophysiology is multifactorial. The factors involved in IBS pathophysiology include visceral hypersensitivity, intestinal dysmotility, psychological factors, dysregulated gut-brain axis, intestinal microbiota alterations, impaired intestinal permeability, and mucosal immune alterations. Recently, mucosal immune alterations have received much attention in IBS. Mast cells are abundant in the intestine, and they communicate with adjacent cells such as epithelial, neuronal, smooth muscle cells or other immune cells through the mediators released when they are activated. Many studies have suggested that mast cells play a role in the pathophysiology of IBS. This review will focus on the role of mast cells in IBS.

• Mast cell activation
• Degranulation
• Irritable bowel syndrome

This study examined whether the densities of stem- and enteroendocrine cell progenitors are abnormal in the ileum of patients with irritable bowel syndrome (IBS), and whether any abnormalities in ileal enteroendocrine cells are correlated with abnormalities in stem cells and enteroendocrine cell progenitors.

One hundred and one IBS patients covering all IBS subtypes were recruited, and 39 non-IBS subjects were included as a control group. The patients and controls underwent standard colonoscopies, during which biopsy specimens were obtained from the ileum. The biopsy specimens were stained with hematoxylin-eosin and immunostained for Musashi-1 (Msi-1), neurogenin 3 (NEUROG3), chromogranin A (CgA), serotonin, peptide YY (PYY), oxyntomodulin (enteroglucagon), pancreatic polypeptide, and somatostatin. The immunoreactive cells were quantified by computerized image analysis.

The densities of Msi-1, NEUROG3, CgA, and serotonin cells were reduced in all IBS patients and in patients with diarrhea-predominant IBS (IBS-D), mixed-diarrhea-and-constipation IBS (IBS-M), and constipation-predominant (IBS-C) relative to the control subjects. While the PYY cell density was increased in IBS-C relative to controls, it did not differ between control subjects and IBS-D and IBS-M patients. The densities of Msi-1 and NEUROG3 cells were strongly correlated with that of CgA cells.

The abnormalities in the ileal enteroendocrine cells appear to be caused by two mechanisms: (1) decreases in the clonogenic activity of the stem cells and in the endocrine-cell progenitors differentiating into enteroendocrine cells, and (2) switching on the expression of PYY and switching off the expression of certain other hormones in other types of the enteroendocrine cells.

• Enteroendocrine cells
• IBS
• Ileum
• Immunohistochemistry
• Mushasi-1
• Neurogenin 3
• PYY
• Serotonin

• Diet
• Musashi-1
• genes
• low-grade inflammation
• microbiota
• neurogenin 3
• stem cells

• T lymphocyte
• cytokine
• enterochromaffin cell
• interleukin
• irritable bowel syndrome
• mast cell

• Cytokines/metabolism
• Enterochromaffin Cells/immunology
• Humans
• Immunity, Mucosal
• Inflammation Mediators/metabolism
• Intestinal Mucosa/immunology
• Irritable Bowel Syndrome/immunology
• Mast Cells/immunology
• T-Lymphocyte Subsets/immunology

• diet
• enteroendocrine cells
• ileum
• image analysis
• immunohistochemistry
• irritable bowel syndrome

• chromogranin A
• genes
• low-grade inflammation
• microbiota
• peptide YY
• somatostatin
• stem cell

• hs-crp
• ibs
• low grade inflammation

• Inflammation
• Irritable bowel syndrome
• Mast cells
• Neuroendocrine cells
• Pathology

• Animals
• Anti-Inflammatory Agents/therapeutic use
• Enteritis/drug therapy
• Enteritis/immunology
• Enteritis/physiopathology
• Gastrointestinal Agents/therapeutic use
• Humans
• Inflammation Mediators/antagonists & inhibitors
• Inflammation Mediators/immunology
• Intestinal Mucosa/drug effects
• Intestinal Mucosa/immunology
• Intestinal Mucosa/innervation
• Intestinal Mucosa/physiopathology
• Irritable Bowel Syndrome/drug therapy
• Irritable Bowel Syndrome/immunology
• Irritable Bowel Syndrome/physiopathology
• Molecular Targeted Therapy

Irritable bowel syndrome (IBS) is a multifactorial functional disorder with no clearly defined etiology or pathophysiology. Modern culture-independent techniques have improved the understanding of the gut microbiota’s composition and demonstrated that an altered gut microbiota profile might be found in at least some subgroups of IBS patients. Research on IBS from a microbial perspective is gaining momentum and advancing. This review will therefore highlight potential links between the gut microbiota and IBS by discussing the current knowledge of the gut microbiota; it will also illustrate bacterial-host interactions and how alterations to these interactions could exacerbate, induce or even help alleviate IBS.

• Dysbiosis
• Immunity
• Irritable bowel syndrome
• Microbiota
• Probiotics

• FUNCTIONAL BOWEL DISORDER
• FUNCTIONAL DYSPEPSIA
• IRRITABLE BOWEL SYNDROME
• MAST CELLS
• NERVE - GUT INTERACTIONS

Irritable bowel syndrome (IBS) is a common gastrointestinal disorder, the pathophysiology of which is not completely known, although it has been shown that genetic/social learning factors, diet, intestinal microbiota, intestinal low-grade inflammation, and abnormal gastrointestinal endocrine cells play a major role. Studies of familial aggregation and on twins have confirmed the heritability of IBS. However, the proposed IBS risk genes are thus far nonvalidated hits rather than true predisposing factors. There is no convincing evidence that IBS patients suffer from food allergy/intolerance, with the effect exerted by diet seemingly caused by intake of poorly absorbed carbohydrates and fiber. Obesity is a possible comorbidity of IBS. Differences in the microbiota between IBS patients and healthy controls have been reported, but the association between IBS symptoms and specific bacterial species is uncertain. Low-grade inflammation appears to play a role in the pathophysiology of a major subset of IBS, namely postinfectious IBS. The density of intestinal endocrine cells is reduced in patients with IBS, possibly as a result of genetic factors, diet, intestinal microbiota, and low-grade inflammation interfering with the regulatory signals controlling the intestinal stem-cell clonogenic and differentiation activities. Furthermore, there is speculation that this decreased number of endocrine cells is responsible for the visceral hypersensitivity, disturbed gastrointestinal motility, and abnormal gut secretion seen in IBS patients.

• Diet
• Endocrine cells
• Genetic factors
• Low-grade inflammation
• Microbiota
• Stem cells

• Animals
• Comorbidity
• Diet/adverse effects
• Gene-Environment Interaction
• Genetic Markers
• Genetic Predisposition to Disease
• Host-Pathogen Interactions
• Humans
• Intestines/microbiology
• Intestines/pathology
• Intestines/physiopathology
• Irritable Bowel Syndrome/etiology
• Irritable Bowel Syndrome/genetics
• Irritable Bowel Syndrome/metabolism
• Irritable Bowel Syndrome/microbiology
• Irritable Bowel Syndrome/physiopathology
• Microbiota
• Phenotype
• Risk Factors
• Signal Transduction
• Stem Cells/metabolism
• Stem Cells/microbiology
• Stem Cells/pathology

Irritable bowel syndrome (IBS) is a common functional gastrointestinal disorder characterized by high prevalence and recurrence rates, which contribute to the patient's poor quality of life and an economic burden to the society and family for substantial costs. Multiple factors (e.g., stress, infection, and food allergy) can induce IBS via the neuro-endocrine-immune system. Abdominal pain, a hallmark symptom of IBS, correlates with visceral hypersensitivity. In recent years, the immune-associated mechanism for IBS has received more and more attention. Mast cells (MCs) are important immune cells in the intestine. The changes in the number, degranulation and interaction of MCs with the nerve play an important role in the development of IBS. This paper reviews the association between mast cells and the onset of IBS.

• Irritable bowel syndrome
• Mast cells
• Degranulation
• Sensory neuron

Irritable bowel syndrome (IBS) is a common chronic gastrointestinal disorder that is characterized by intermittent abdominal pain/discomfort, altered bowel habits and abdominal bloating/distension. This review aimed at presenting the recent developments concerning the role of diet in the pathophysiology and management of IBS. There is no convincing evidence that IBS patients suffer from food allergy/intolerance, and there is no evidence that gluten causes the debated new diagnosis of non-coeliac gluten sensitivity (NCGS). The component in wheat that triggers symptoms in NCGS appears to be the carbohydrates. Patients with NCGS appear to be IBS patients who are self-diagnosed and self-treated with a gluten-free diet. IBS symptoms are triggered by the consumption of the poorly absorbed fermentable oligo-, di-, monosaccharides and polyols (FODMAPs) and insoluble fibre. On reaching the distal small intestine and colon, FODMAPS and insoluble fibre increase the osmotic pressure in the large-intestine lumen and provide a substrate for bacterial fermentation, with consequent gas production, abdominal distension and abdominal pain or discomfort. Poor FODMAPS and insoluble fibres diet reduces the symptom and improve the quality of life in IBS patients. Moreover, it changes favourably the intestinal microbiota and restores the abnormalities in the gastrointestinal endocrine cells. Five gastrointestinal endocrine cell types that produce hormones regulating appetite and food intake are abnormal in IBS patients. Based on these hormonal abnormalities, one would expect that IBS patients to have increased food intake and body weight gain. However, the link between obesity and IBS is not fully studied. Individual dietary guidance for intake of poor FODMAPs and insoluble fibres diet in combination with probiotics intake and regular exercise is to be recommended for IBS patients.

We aim to report the prevalence of irritable bowel syndrome (IBS) and elucidate the influence of IBS on the incidence of colorectal neoplasm through a community-screening-based, longitudinal follow-up study.

We enroled 39 384 community residents aged 40 years or older who had participated in a community-based colorectal cancer-screening programme with an immunochemical faecal occult test since 1999. We followed a cohort that was free of colorectal neoplasm (excluding colorectal neoplasm at baseline) to ascertain the incident colorectal neoplasm through each round of screening and used a nationwide cancer registry. Information on IBS was obtained by linking this screened cohort with population-based health insurance claim data. Other confounding factors were also collected via questionnaire or biochemical tests.

The overall period prevalence of IBS was 23%, increasing from 14.7% for subjects aged 40–49 years to 43.7% for those aged 70 years and more. After controlling for age, gender and family history of colorectal cancer, screenees who had been diagnosed as having IBS exhibited a significantly elevated level (21% adjusted hazard ratio (HR)=1.21 (95% CI: 1.02–1.42)) of incident colorectal adenoma compared with those who had not been diagnosed with IBS. A similar finding was noted for invasive carcinoma; however, the size of the effect was of borderline statistical significance (adjusted HR=1.20 (95% CI: 0.94–1.53)).

IBS led to an increased risk for incident colorectal neoplasm.

To the best of our knowledge, stomach antral endocrine cells have not previously been investigated in patients with irritable bowel syndrome (IBS). Thus, in the present study, 76 patients with IBS were examined (designated as IBS-total). Diarrhoea was the predominant symptom in 26 of these patients (IBS-D), while in 21 patients, the predominant symptoms were both diarrhoea and constipation (IBS-M) and in 29 patients the predominant symptom was constipation (IBS-C). Forty-three healthy subjects were enrolled as the controls. Stomach antral biopsy samples obtained from all of the subjects were immunostained using the avidin-biotin-complex method for serotonin, gastrin, somatostatin and serotonin transporter (SERT). The immunopositive cell densities and immunoreactivity intensities were determined by computer-aided image analysis. The density of the serotonin-immunoreactive cells was significantly decreased in the IBS-M patients and increased in the IBS-C patients relative to the controls. The immunoreactivity intensity did not differ significantly between the controls and IBS-total. The density of the gastrin-immunoreactive cells was significantly greater in the IBS-D, IBS-M and IBS-C patients than in the controls. The immunoreactivity intensity of gastrin was significantly greater in the IBS-D patients than in the controls. The density of the somatostatin-immunoreactive cells cells was significantly lower in the IBS-total, IBS-D, IBS-M and IBS-C patients than in the controls. The immunoreactivity intensities of both somatostatin and SERT did not differ significantly between the controls and IBS-total. The increase in gastrin cell density and the decrease in somatostatin cell density in all IBS subtypes may cause high levels of gastric secretion, which may in turn contribute to the high incidence of dyspepsia and gastro-oesophageal reflux observed in patients with IBS.

Enteroendocrine cells (EEC) are highly specialized cells producing signalling molecules vital to the normal functions of the gut. Recently, we showed altered protein distribution in Chlamydia infected EEC in vitro. The aim of this study was to perform a microarray analysis of the response pattern of EEC from both large and small bowel to infection in vitro, using Chlamydia trachomatis infection as a model.

Two human EEC lines: LCC-18, derived from a neuroendocrine colonic tumour, and CNDT-2, derived from a small intestinal carcinoid, were infected using cultured C. trachomatis serovar LGV II strain 434 (ATCC VR-902B). Penicillin G was used to induce persistent infection. We used microarray analysis (Affymetrix GeneChip®) for studying changes in gene expression at different stages of infection.

Twenty-four hours after active and persistent infection, 66 and 411 genes in LCC-18 and 68 and 170 genes in CNDT-2 cells, respectively showed mean expression ratios >2-fold compared to non-infected cells. These genes encoded factors regulating apoptosis, cell differentiation, transcription regulation, cytokine activity, amine biosynthesis and vesicular transport. We found significant differences in gene transcription levels between persistently infected and non-infected cells in 10 genes coding for different solute carrier transporters (SLC) and in 5 genes related to endocrine function (GABARAPL1, GRIP1, DRD2, SYT5 and SYT7).

Infected EEC cells exhibit cell-type specific patterns related to vesicular transport, secretion and neurotransmitters. EEC play a pivotal role in regulation of gut motility and an impairment of enteroendocrine function can contribute to motility disorders.

• Chlamydia trachomatis
• Enteroendocrine cells
• Infection
• Microarray

• irritable bowel syndrome
• pathogenesis
• peripheral mechanisms

• Adultos
• Adults
• Antibiotic treatment
• Bacteria overgrowth
• Children
• Inflamación de bajo grado
• Irritable bowel syndrome
• Low-grade inflammation
• Microbiota
• Niños
• Post-infectious
• Postinfeccioso
• Revisión sistemática basada en evidencias
• Rifaximin
• Rifaximina
• Sobrepoblación bacteriana
• Systematic evidence-based review
• Síndrome de intestino irritable
• Tratamiento con antibióticos

• Evidence-Based Medicine
• Gastrointestinal Diseases/microbiology
• Gastrointestinal Diseases/pathology
• Humans
• Irritable Bowel Syndrome/microbiology
• Irritable Bowel Syndrome/pathology
• Microbiota

• Computer image analysis
• Ileum
• Irritable bowel syndrome
• Peptide YY
• Serotonin

• Adolescent
• Adult
• Aged
• Biomarkers/analysis
• Biopsy
• Case-Control Studies
• Colonoscopy
• Constipation/etiology
• Diarrhea/etiology
• Endocrine Cells/chemistry
• Endocrine Cells/pathology
• Female
• Glucagon-Like Peptides/analysis
• Humans
• Hyperalgesia/etiology
• Ileum/chemistry
• Ileum/pathology
• Image Interpretation, Computer-Assisted
• Immunohistochemistry
• Irritable Bowel Syndrome/complications
• Irritable Bowel Syndrome/metabolism
• Irritable Bowel Syndrome/pathology
• Male
• Middle Aged
• Pain Measurement
• Pancreatic Polypeptide/analysis
• Peptide YY/analysis
• Serotonin/analysis
• Somatostatin/analysis
• Somatostatin-Secreting Cells/chemistry
• Somatostatin-Secreting Cells/pathology
• Surveys and Questionnaires
• Visceral Pain/etiology
• Young Adult

• Campylobacter jejuni
• barrier function
• gut permeability
• infectious gastroenteritis
• postinfectious irritable bowel syndrome

• Afferent nerves
• Chronic pain
• Inflammatory bowel disease
• Irritable bowel syndrome
• Sensitisation
• Sensory nerves
• Visceral hypersensitivity

• Abdominal Pain/pathology
• Abdominal Pain/physiopathology
• Afferent Pathways/pathology
• Afferent Pathways/physiopathology
• Animals
• Enteric Nervous System/pathology
• Enteric Nervous System/physiopathology
• Gastrointestinal Tract/innervation
• Humans
• Hyperalgesia/pathology
• Hyperalgesia/physiopathology
• Inflammatory Bowel Diseases/pathology
• Inflammatory Bowel Diseases/physiopathology
• Irritable Bowel Syndrome/pathology
• Irritable Bowel Syndrome/physiopathology
• Pain Perception
• Pain Threshold

Irritable bowel syndrome (IBS) is a common gastrointestinal disorder that is generally considered to be functional because there appears to be no associated anatomical defect. Stress and psychological factors are thought to play an important role in IBS. The gut neuroendocrine system (NES), which regulates all functions of the gastrointestinal tract, consists of endocrine cells that are scattered among the epithelial cells of the mucosa, and the enteric nervous system. Although it is capable of operating independently from the central nervous system (CNS), the gut NES is connected to and modulated by the CNS. This review presents evidence for the presence of an anatomical defect in IBS patients, namely in the gastrointestinal endocrine cells. These cells have specialized microvilli that project into the lumen and function as sensors for the luminal content and respond to luminal stimuli by releasing hormones into the lamina propria, which starts a chain reaction that progresses throughout the entire NES. The changes in the gastrointestinal endocrine cells observed in IBS patients are highly consistent with the other abnormalities reported in IBS patients, such as visceral hypersensitivity, dysmotility, and abnormal secretion.

• Cholecystokinin
• Dysmotility
• Endocrine cells
• Enteric nervous system
• Ghrelin
• Peptide YY
• Secretion
• Secretin
• Serotonin
• Visceral hypersensitivity

• Abdominal Pain/etiology
• Abdominal Pain/metabolism
• Animals
• Colon/innervation
• Colon/metabolism
• Colon/pathology
• Enteroendocrine Cells/metabolism
• Enteroendocrine Cells/pathology
• Gastrointestinal Motility
• Humans
• Irritable Bowel Syndrome/diagnosis
• Irritable Bowel Syndrome/etiology
• Irritable Bowel Syndrome/metabolism
• Irritable Bowel Syndrome/physiopathology
• Neuroendocrine Cells/metabolism
• Neuroendocrine Cells/pathology
• Risk Factors
• Signal Transduction

• Computerised image analysis
• Enteroglucagon
• PYY
• Rectum
• Serotonin
• Somatostatin

• Adolescent
• Adult
• Cell Count
• Endocrine Cells/metabolism
• Female
• Humans
• Irritable Bowel Syndrome/metabolism
• Irritable Bowel Syndrome/pathology
• Male
• Middle Aged
• Oxyntomodulin/metabolism
• Peptide YY/metabolism
• ROC Curve
• Rectum/pathology
• Serotonin/metabolism
• Somatostatin/metabolism
• Young Adult

In the present study, post inflammation irritable bowel syndrome (PI-IBS) rats were firstly established by intracolonic instillation of acetic acid with restraint stress. Then the pharmacokinetics of berberine in the rat plasma were compared after oral administration of berberine hydrochloride (25 mg/kg) to normal rats and PI-IBS rats. Quantification of berberine in the rat plasma was achieved by using a sensitive and rapid UPLC-MS/MS method. Plasma samples were collected at 15 different points in time and the pharmacokinetic parameters were analyzed by WinNonlin software. Compared with the normal group, area under the plasma concentration vs. time curve from zero to last sampling time (AUC_0–t) and total body clearance (CL/F) in the model group significantly increased or decreased, (2039.49 ± 492.24 vs. 2763.43 ± 203.14; 4999.34 ± 1198.79 vs. 3270.57 ± 58.32) respectively. The results indicated that the pharmacokinetic process of berberine could be altered in PI-IBS pathological conditions.

• campylobacter jejuni
• functional gi disorders
• infectious gastroenteritis
• irritable bowel syndrome
• post-infectious irritable bowel syndrome

• gastrointestinal
• inflammation
• microbiota

• Humans
• Intestines/immunology
• Intestines/microbiology
• Irritable Bowel Syndrome/microbiology

• DK075621 NIDDK NIH HHS
• DK084294 NIDDK NIH HHS

Irritable bowel syndrome (IBS) is a common chronic functional gastrointestinal disorder. Post-infectious IBS (PI-IBS) is a subset of IBS that accounts for a large proportion of IBS patients. The PI-IBS symptoms meet the Rome criteria for IBS with diarrhoea (IBS-D) or IBS with mixed bowel habits (IBS-M). A low-grade inflammation has been reported to occur in PI-IBS. Abnormalities in intestinal endocrine cells have been reported in both sporadic IBS and PI-IBS.

A 20-year-old female with a diagnosis of IBS with constipation (IBS-C), according to Rome III criteria, contracted Campylobacter-induced gastroenteritis, after which her symptom pattern changed to IBS-M. She showed an intestinal low-grade inflammation that was manifested by an increase in the number of intraepithelial and lamina propria leucocytes and lymphocytes and an increase in the density of mast cells in lamina propria. There was also an increase in the density of intestinal serotonin and peptide YY (PYY) cells and a decrease in the density of rectal somatostatin cells. Follow-up of the patient at 4-months post-infection revealed reduction of IBS symptoms and an improvement in her quality of life. However, 6 months following the Campylobacter infection, the patient switched back from IBS-M to IBS-C, probably due to recovery from PI-IBS. The patient was treated with prucalopride, which is serotonin 5HT₄ receptor agonist. Six months later following this treatment, the symptoms were reduced and the quality of life improved in the reported patient.

Gastroenteritis in patients with IBS-C causes a post-infectious, low-grade inflammation. Interaction between immune-cells and intestinal endocrine cells increases the density of certain endocrine cells, which in turn might be responsible for the change in the symptom pattern, the milder symptoms and the improvement in the quality of life seen in the reported patient. The findings in this case raise the question as to whether intestinal infections are responsible for the previously reported switching of IBS from one subtype to another over time.