Abstract
BackgroundMicrobial dysbiosis and prolonged immune activation resulting in low-grade inflammation and intestinal barrier dysfunction have been suggested to be underlying causes of post-infectious irritable bowel syndrome (PI-IBS). The aim of this study was to evaluate the difference in cytokine response between mucosal specimens of PI-IBS patients and healthy controls (HC) after ex vivo stimulation with key anaerobic bacteria.MethodsColonic biopsies from 11 PI-IBS patients and 10 HC were stimulated ex vivo with the commensal bacteria Bacteroides ovatus, Ruminococcus gnavus, Akkermansia muciniphila, Subdoligranulum variabile and Eubacterium limosum, respectively. The cytokine release (IL-1β, IL-2, IL-8, IL-10, IL-13, IL-17, TNF-α and IFN-γ) in stimulation supernatants was analyzed using the LUMINEX assay. Comparison of cytokine release between PI-IBS patients and healthy controls was performed taking both unstimulated and bacterially stimulated mucosal specimens into account.Key ResultsIL-13 release from mucosal specimens without bacterial stimulation was significantly lower in PI-IBS patients compared to HC (p < 0.05). After stimulation with Subdoligranulum variabile, IL-1β release from PI-IBS patients was significantly increased compared to HC (p < 0.05). Stimulation with Eubacterium limosum resulted in a significantly decreased IL-10 release in HC compared to PI-IBS patients (p < 0.05) and a tendency to decreased IL-13 release in HC compared to PI-IBS patients (p = 0.07).Conclusions & InferencesPI-IBS patients differ from HC with regard to cytokine release ex vivo after stimulation with selected commensal bacteria. Hence, our results support that the pathogenesis of PI-IBS comprises an altered immune response against commensal gut microbes.
Highlights
Irritable bowel syndrome (IBS) is a functional gastrointestinal disorder characterized by chronic abdominal symptoms, including discomfort, pain and altered bowel habits
postinfectious irritable bowel syndrome (PI-IBS) patients differ from healthy controls (HC) with regard to cytokine release ex vivo after stimulation with selected commensal bacteria
Baseline IL-13 release from biopsies without bacterial stimulation was significantly lower in PI-IBS patients compared to healthy controls. showed no significant difference The release of the other cytokines (i.e. IL-1β, IL-2, IL-8, IL-10, IL-17, TNF-α or IFN-γ) in biopsies without prior bacterial stimulation did not significantly differ between PI-IBS patients and healthy controls (Table 2)
Summary
Irritable bowel syndrome (IBS) is a functional gastrointestinal disorder characterized by chronic abdominal symptoms, including discomfort, pain and altered bowel habits. Even though the pathophysiology of IBS and PI-IBS is still not clarified, prolonged immune activation resulting in microbial dysbiosis [2,3,4], low-grade inflammation [5, 6], and intestinal barrier dysfunction [7] has been suggested to be underlying causes. The majority of studies that show alterations of the intestinal immune system and/or microbiota in IBS patients are strictly descriptive, which limits the elucidation of a temporal association between putative causes and pathophysiological effects. Mucosal immune activation has been associated with deterioration of the integrity of the epithelial barrier and intestinal dysfunction in IBS [10, 11]. Microbial dysbiosis and prolonged immune activation resulting in low-grade inflammation and intestinal barrier dysfunction have been suggested to be underlying causes of postinfectious irritable bowel syndrome (PI-IBS). The aim of this study was to evaluate the difference in cytokine response between mucosal specimens of PI-IBS patients and healthy controls (HC) after ex vivo stimulation with key anaerobic bacteria
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