PTH-034 Stress-induced immunomodulation in irritable bowel syndrome suppresses Th1 and Th2 cytokines

Abstract

Introduction Stress induced immunomodulation has evolved to confer maximum biological advantage to an organism exposed to varying environmental stressors. Stress is also implicated in the aetiology of Irritable Bowel Syndrome (IBS). Herein, we examined the immunophenotype of IBS patients for evidence of stress related immunomodulation. Methods 24-IBS patients and 9-matched controls subjects were studied. Comprehensive clinical, psychological (eg, somatisation) and symptomatic (eg, Visceral Sensitivity Index (VSI)) evaluations were performed. Peripheral blood mononuclear cells (PBMC9s) were stimulated using lipopolysacharide (5-concentrations) in the presence or absence of exogenous corticotrophin releasing hormone (CRH). A broad panel of inflammatory markers were measured in the supernatant. A one-way ANOVA was performed and data reported as point estimates of difference, 95% CI (IBS-Controls). Results Levels of IL2 (−44.5 (−66 to −22) p Conclusion As seen in chronic stress, IBS patients suppress Th1 and Th2 cytokine release from stimulated PBMC9s and this suppression is negatively correlated with increasing symptom severity and psychological comorbidity. Elevation of IL-6, and suppression of IFN-γ, IL-2 and IL-4 may indicate a shift towards a TH17 immune profile. This immunophenotype would convey a biological advantage in terms of enhanced mucosal host defence but may also establish a pro-inflammatory mucosal cytokine profile which would promote gastrointestinal symptoms. The potential interaction between stress and TH17 immune function in IBS could represent a new insight in IBS pathophysiology.