Disturbed in vitro adrenergic modulation of cytokine production in inflammatory bowel diseases in remission

ObjectivePsychological stress has been implicated in the pathophysiology of both inflammatory and functional gastrointestinal (GI) diseases. The goal of this study was to address neuroendocrine modulation of cytokine production by peripheral blood cells in GI diseases.MethodsWe analyzed the in vitro effects of the β-adrenergic agonist terbutaline and the glucocorticoid agonist dexamethasone on TNF-α and IL-10 production by LPS-stimulated monocytes in whole cell blood cultures in patients with inflammatory bowel diseases in remission (N = 10), diarrhoea-predominant irritable bowel syndrome (IBS, N = 12), patients with a recent gastroenteritis (post-infectious group, N = 10), and healthy controls (N = 15).ResultsIn response to terbutaline, there was a significant increase in IL-10 production (concentration effect: p < 0.05), which was diminished in IBD (group effect: p < 0.01), comparable in IBS and controls, but enhanced in the post-infectious group (group x concentration effect: p < 0.05). In contrast, terbutaline resulted in a concentration-dependent suppression of TNF-α production, which was comparable in all groups. Dexamethasone suppressed TNF-α production in a dose-dependent manner in all groups, but this effect was significantly more pronounced in post-infectious subjects (group effect: p < 0.05).ConclusionsIn IBD, disturbed adrenergic regulation of IL-10 could be part of the mechanism(s) underlying the modulation of disease activity by psychological stress. Diarrhoea-predominant IBS was not associated with altered adrenergic or glucocorticoid regulation of cytokine production by peripheral blood cells, whereas a recent history of gastroenteritis was associated with disturbed neuroendocrine modulation of cytokine production, which may play role in the pathophysiology of post-infectious IBS.