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首页> 美国卫生研究院文献>other >CYTOKINE-INDUCED ALTERATIONS OF α7 NICOTINIC RECEPTOR IN COLONIC CD4 T CELLS MEDIATE DICHOTOMOUS RESPONSE TO NICOTINE IN MURINE MODELS OF Th1/Th17 VS. Th2-MEDIATED COLITIS
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CYTOKINE-INDUCED ALTERATIONS OF α7 NICOTINIC RECEPTOR IN COLONIC CD4 T CELLS MEDIATE DICHOTOMOUS RESPONSE TO NICOTINE IN MURINE MODELS OF Th1/Th17 VS. Th2-MEDIATED COLITIS

机译：细胞因子诱导的α7烟碱受体在结肠CD4 T细胞中的改变介导对Th1 / Th17的鼠模型中的尼古丁的二分法反应。 Th2介导的结肠炎

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Ulcerative colitis (UC) and Crohn’s disease (CD) are two forms of chronic inflammatory bowel disease. CD4 T cells play a central role in the pathogenesis of both diseases. Smoking affects both UC and CD but with opposite effects, ameliorating UC and worsening CD. We hypothesized that the severity of gut inflammation could be modulated through T-cell nicotinic acetylcholine receptors (nAChRs) and that the exact clinical outcome would depend on the repertoire of nAChRs on CD4 T cells mediating each form of colitis. We measured clinical and immunologic outcomes of treating BALB/c mice with oxazolone- and TNBS-induced colitides by nicotine. Nicotine attenuated oxazolone colitis, which was associated with increased percentage of colonic Tregs and a reduction of Th17 cells. TCR stimulation of naïve CD4+CD62L+ T cells in the presence of nicotine upregulated expression of Foxp3. In marked contrast, nicotine worsened TNBS colitis, and this was associated with increased Th17 cells among colonic CD4 T cells. Nicotine upregulated IL-10 and inhibited IL-17 production, which could be abolished by exogenous IL-12 that also abolished the nicotine-dependent upregulation of Tregs. The dichotomous action of nicotine resulted from the up- and downregulation of anti-inflammatory α7 nAChR on colonic CD4 T cells induced by cytokines characteristic of the inflammatory milieu in oxazolone (IL-4), and TNBS (IL-12) colitis, respectively. These findings help explain the dichotomous effect of smoking in patients with UC and CD, and underscore the potential for nicotinergic drugs in regulating colonic inflammation.

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