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Stressor exposure increases colonic inflammation. Because inflammation leads to anxiety-like behavior, we tested whether stressor exposure in mice recovering from dextran-sulfate-sodium (DSS)-induced colitis enhances anxiety-like behavior. Mice received 2% DSS for five consecutive days prior to being exposed to a social-disruption (SDR) stressor (or being left undisturbed). After stressor exposure, their behavior was tested and colitis was assessed via histopathology and via inflammatory-cytokine measurement in the serum and colon. Cytokine and chemokine mRNA levels in the colon, mesenteric lymph nodes (MLNs), hippocampus, and amygdala were measured with RT-PCR. SDR increased anxiety-like behaviors, which correlated with serum and hippocampal IL-17A. The stressor also reduced <i>IL-1β</i>, <i>CCL2</i>, and <i>iNOS</i> in the colonic tissue, but increased <i>iNOS</i>, <i>IFNγ</i>, <i>IL-17A</i>, and <i>TNFα</i> in the MLNs. A network analysis indicated that reductions in colonic <i>iNOS</i> were related to elevated MLN <i>iNOS</i> and <i>IFNγ</i>. These inflammatory markers were related to serum and hippocampal IL-17A and associated with anxiety-like behavior. Our data suggest that <i>iNOS</i> may protect against extra-colonic inflammation, and when suppressed during stress it is associated with elevated MLN <i>IFNγ</i>, which may coordinate gut-to-brain inflammation. Our data point to hippocampal <i>IL-17A</i> as a key correlate of anxiety-like behavior.