Gut microbiota and intestinal immunity—A crosstalk in irritable bowel syndrome

Abstract

Irritable bowel syndrome (IBS), one of the most prevalent functional gastrointestinal disorders, is characterized by recurrent abdominal pain and abnormal defecation habits, resulting in a severe healthcare burden worldwide. The pathophysiological mechanisms of IBS are multi‐factorially involved, including food antigens, visceral hypersensitivity reactions, and the brain–gut axis. Numerous studies have found that gut microbiota and intestinal mucosal immunity play an important role in the development of IBS in crosstalk with multiple mechanisms. Therefore, based on existing evidence, this paper elaborates that the damage and activation of intestinal mucosal immunity and the disturbance of gut microbiota are closely related to the progression of IBS. Combined with the application prospect, it also provides references for further in‐depth exploration and clinical practice.

Exploring the Contribution of Campylobacter jejuni to Post-Infectious Irritable Bowel Syndrome: A Literature Review

“…A significant adverse outcome following infection with C. jejuni is the onset of irritable bowel syndrome (IBS), initially identified by Spiller and associates in 2000, which is linked to intensified activation of enteroendocrine cells (EC) [1]. The recognition of irritable bowel syndrome (IBS) following acute infectious enteritis has been extensively documented across numerous studies [17,19]. However, it was not until 1962 that the notion of PI-IBS was formally introduced into the scientific literature [17,19].…”

“…IBS affects 10-20% of the population, with around 10% of individuals developing PI-IBS following a C. jejuni infection [1,17]. Delineating the specific pathomechanisms underlying PI-IBS is challenging, especially due to the combinations of its various forms [1,17].…”

“…IBS affects 10-20% of the population, with around 10% of individuals developing PI-IBS following a C. jejuni infection [1,17]. Delineating the specific pathomechanisms underlying PI-IBS is challenging, especially due to the combinations of its various forms [1,17]. In 2019, due to the absence of sensitive and specific markers for diagnosis, the Rome Foundation Working Group introduced symptomatic diagnostic criteria for PI-IBS, leveraging the Rome IV guidelines [7].…”

“…The reported incidence of PI-IBS stands at ≈20% under the Rome III criteria, whereas the Rome IV criteria suggest a slightly lower incidence rate of between 10% and 12.8% [18]. Based on the predominant bowel pattern, as measured by the Bristol stool scale, PI-IBS classifications were proposed, including most common mixed (IBS-M), diarrhea-dominant (IBS-D) and constipation-dominant (IBS-C) [1,7,17]. Beyond the three primary clinical forms, additional research has identified three distinct variants of IBS: pain-predominant IBS (P-IBS), PI-IBS and post-diverticulitis (IBS-PD).…”

Chronic Gut Inflammation and Dysbiosis in IBS: Unraveling Their Contribution to Atopic Dermatitis Progression

“…Research indicates that in conditions such as IBS, gut inflammation can lead to increased intestinal permeability. This change allows for microbial products and pro-inflammatory cytokines to enter the systemic circulation, possibly contributing to widespread inflammation [ 9 ]. This mechanism can exacerbate conditions like AD.…”