Lomax Alan E, Pradhananga Sabindra, Bertrand Paul P
Gastrointestinal Disease Research Unit, Queen's University, Kingston, Ontario, Canada; and
Gastrointestinal Disease Research Unit, Queen's University, Kingston, Ontario, Canada; and.
Am J Physiol Gastrointest Liver Physiol. 2017 Mar 1;312(3):G165-G170. doi: 10.1152/ajpgi.00365.2016. Epub 2017 Jan 12.
Altered gastrointestinal (GI) function contributes to the debilitating symptoms of inflammatory bowel diseases (IBD). Nerve circuits contained within the gut wall and outside of the gut play important roles in modulating motility, mucosal fluid transport, and blood flow. The structure and function of these neuronal populations change during IBD. Superimposed on this plasticity is a diminished responsiveness of effector cells - smooth muscle cells, enterocytes, and vascular endothelial cells - to neurotransmitters. The net result is a breakdown in the precisely orchestrated coordination of motility, fluid secretion, and GI blood flow required for health. In this review, we consider how inflammation-induced changes to the effector innervation of these tissues, and changes to the tissues themselves, contribute to defective GI function in models of IBD. We also explore the evidence that reversing neuronal plasticity is sufficient to normalize function during IBD.
胃肠道（GI）功能改变会导致炎症性肠病（IBD）出现使人虚弱的症状。肠壁内和肠外的神经回路在调节运动、粘膜液体运输和血流方面发挥着重要作用。在IBD期间，这些神经元群体的结构和功能会发生变化。叠加在这种可塑性之上的是效应细胞（平滑肌细胞、肠上皮细胞和血管内皮细胞）对神经递质的反应性降低。最终结果是健康所需的运动、液体分泌和胃肠道血流的精确协调受到破坏。在这篇综述中，我们探讨炎症如何引起这些组织效应器神经支配的变化以及组织自身的变化，进而导致IBD模型中胃肠道功能缺陷。我们还探讨了相关证据，即逆转神经元可塑性足以使IBD期间的功能恢复正常。
