BACKGROUND & AIMS: Recent studies suggest that life events and chronic stress increase the risk of relapse in inflammatory bowel disease. Our aim was to study the effects of acute psychologic stress on systemic and rectal mucosal inflammatory responses in patients with inactive ulcerative colitis (UC). METHODS: Twenty-five patients with inactive UC and 11 healthy volunteers (HV) underwent an experimental stress test. Ten patients with UC and 11 HV underwent a control procedure. Before and after each procedure, systemic inflammatory response was assessed by serum interleukin (IL)-6 and IL-13 concentrations, tumor necrosis factor (TNF)-alpha and IL-6 production by lipopolysaccharide (LPS)-stimulated whole blood, leukocyte count, natural killer (NK) cell numbers, platelet activation, and platelet-leukocyte aggregate (PLA) formation. In patients with UC, rectal mucosal inflammation was assessed by TNF-alpha, IL-13, histamine and substance P release, reactive oxygen metabolite (ROM) production, mucosal blood flow (RMBF) and histology. RESULTS: Stress increased pulse (P < .0001) and systolic BP (P < .0001). In UC, stress increased LPS-stimulated TNF-alpha and IL-6 production by 54% (P = .004) and 11% (P = .04), respectively, leukocyte count by 16% (P = .01), NK cell count by 18% (P = .0008), platelet activation by 65% (P < .0001), PLA formation by 25% (P = .004), mucosal TNF-alpha release by 102% (P = .03), and ROM production by 475% (P = .001) and reduced rectal mucosal blood flow by 22% (P = .05). The control protocol did not change any of the variables measured. There were no differences between the responses of the patients with UC and HV. CONCLUSIONS: Acute psychologic stress induces systemic and mucosal proinflammatory responses, which could contribute to exacerbations of UC in ordinary life.
BACKGROUND & AIMS: Recent studies suggest that life events and chronic stress increase the risk of relapse in inflammatory bowel disease. Our aim was to study the effects of acute psychologic stress on systemic and rectal mucosal inflammatory responses in patients with inactive ulcerative colitis (UC). METHODS: Twenty-five patients with inactive UC and 11 healthy volunteers (HV) underwent an experimental stress test. Ten patients with UC and 11 HV underwent a control procedure. Before and after each procedure, systemic inflammatory response was assessed by serum interleukin (IL)-6 and IL-13 concentrations, tumor necrosis factor (TNF)-alpha and IL-6 production by lipopolysaccharide (LPS)-stimulated whole blood, leukocyte count, natural killer (NK) cell numbers, platelet activation, and platelet-leukocyte aggregate (PLA) formation. In patients with UC, rectal mucosal inflammation was assessed by TNF-alpha, IL-13, histamine and substance P release, reactive oxygen metabolite (ROM) production, mucosal blood flow (RMBF) and histology. RESULTS: Stress increased pulse (P < .0001) and systolic BP (P < .0001). In UC, stress increased LPS-stimulated TNF-alpha and IL-6 production by 54% (P = .004) and 11% (P = .04), respectively, leukocyte count by 16% (P = .01), NK cell count by 18% (P = .0008), platelet activation by 65% (P < .0001), PLA formation by 25% (P = .004), mucosal TNF-alpha release by 102% (P = .03), and ROM production by 475% (P = .001) and reduced rectal mucosal blood flow by 22% (P = .05). The control protocol did not change any of the variables measured. There were no differences between the responses of the patients with UC and HV. CONCLUSIONS: Acute psychologic stress induces systemic and mucosal proinflammatory responses, which could contribute to exacerbations of UC in ordinary life.
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