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首页> 外文期刊>American Journal of Physiology >Proinflammatory cytokines alter/reduce esophageal circular muscle contraction in experimental cat esophagitis.
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Proinflammatory cytokines alter/reduce esophageal circular muscle contraction in experimental cat esophagitis.

机译：在实验性猫食管炎中，促炎细胞因子改变/减少了食管环形肌的收缩。

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摘要

Cholinergic mechanisms are largely responsible for esophageal contraction in response to swallowing or to in vitro electrical field stimulation (EFS). After induction of experimental esophagitis by repeated acid perfusion, the responses to swallowing and to EFS were significantly reduced but contraction in response to ACh was not affected, suggesting that cholinergic mechanisms are damaged by acid perfusion but that myogenic mechanisms are not. Measurements of ACh release in response to EFS confirmed that release of ACh was reduced in esophagitis compared with normal controls. To examine factors contributing to this neuropathy, normal esophageal strips were incubated for 1-2 h with the proinflammatory cytokines IL-1beta (100 U/ml), IL-6 (1 ng/ml), or TNF-alpha (1 ng/ml). IL-1beta and IL-6 levels, measured by Western blot analysis, increased in esophagitis compared with normal circular muscle. IL-1beta and IL-6 reduced contraction in response to EFS (2-10 Hz, 0.2 ms) but did not affect ACh-induced contraction, suggesting that these cytokines inhibit ACh release without affecting myogenic contractile mechanisms. EFS-induced ACh release was significantly reduced in normal esophageal strips by incubation in IL-1beta or IL-6, suggesting that they may contribute to the contractility changes. TNF-alpha at 1 ng/ml, however, did not affect the response to ACh or to electrical stimulation but inhibited both at higher concentrations. TNF-alpha levels were low in normal muscle and did not increase with esophagitis. The data suggest that the proinflammatory cytokines IL-1beta and IL-6 contribute to reduced esophageal contraction by inhibiting release of ACh from myenteric neurons.
机译：胆碱能机制是吞咽或体外电场刺激（EFS）引起食管收缩的主要原因。通过反复的酸灌流诱发实验性食管炎后，吞咽和EFS的反应显着降低，但对ACh的反应收缩却未受影响，这表明酸灌流损害了胆碱能机制，但肌原性机制并未受到损害。响应EFS的ACh释放的测量结果证实，与正常对照组相比，食管炎中ACh的释放减少了。为了检查促成这种神经病的因素，将正常食管条与促炎细胞因子IL-1beta（100 U / ml），IL-6（1 ng / ml）或TNF-alpha（1 ng / ml）孵育1-2小时毫升）。与正常的环形肌相比，食管炎中通过蛋白质印迹分析测得的IL-1beta和IL-6水平升高。 IL-1beta和IL-6减少了对EFS的收缩（2-10 Hz，0.2 ms），但不影响ACh诱导的收缩，表明这些细胞因子抑制ACh释放而不影响肌源性收缩机制。通过在IL-1beta或IL-6中孵育，正常食管条带中EFS诱导的ACh释放显着减少，表明它们可能有助于收缩力变化。然而，1 ng / ml的TNF-α不会影响对ACh或电刺激的反应，但在较高浓度下均能抑制。正常肌肉中的TNF-α水平较低，并没有因食管炎而升高。数据表明，促炎细胞因子IL-1beta和IL-6通过抑制ACh从肌层神经元的释放而有助于减少食道收缩。

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