美国洛克菲勒大学Daniel Mucida、Tomasz Ahrends等研究人员合作发现，肠道病原体诱导组织耐受并防止随后感染引起的神经元损失。2021年10月29日，国际知名学术期刊《细胞》在线发表了这一成果。
研究人员报道了病原体暴露后防止神经元损失和肠道运动破坏的潜在耐受机制。结果表明，在肠道感染后，肌肉巨噬细胞（MM）获得了一种组织保护表型，可以防止神经元损失、运动障碍，并在随后感染无关病原体时保持能量平衡。细菌诱导的神经保护依赖于激活肠道投射的交感神经元和通过MM上的β2-肾上腺素能受体（β2AR）发出信号。相反，蠕虫介导的神经保护依赖于T细胞和嗜酸性粒细胞产生的白细胞介素（IL）-4和IL-13，这能够诱导表达精氨酸酶的MM，防止位于不同肠道区域的不相关感染造成的神经元损失。
总之，这些数据表明，不同的肠道病原体引发了一种疾病或组织耐受状态，从而保留了肠道神经系统（ENS）的数量和功能。
据了解，ENS控制着一些肠道功能，包括运动和营养物质的处理，这些功能可被感染引起的神经病变或神经元细胞死亡所破坏。
附：英文原文
Title: Enteric pathogens induce tissue tolerance and prevent neuronal loss from subsequent infections
Author: Tomasz Ahrends, Begüm Aydin, Fanny Matheis, Cajsa H. Classon, Franois Marchildon, Gláucia C. Furtado, Sérgio A. Lira, Daniel Mucida
Issue&Volume: 2021-10-29
Abstract: The enteric nervous system (ENS) controls several intestinal functions including motilityand nutrient handling, which can be disrupted by infection-induced neuropathies orneuronal cell death. We investigated possible tolerance mechanisms preventing neuronalloss and disruption in gut motility after pathogen exposure. We found that followingenteric infections, muscularis macrophages (MMs) acquire a tissue-protective phenotypethat prevents neuronal loss, dysmotility, and maintains energy balance during subsequentchallenge with unrelated pathogens. Bacteria-induced neuroprotection relied on activationof gut-projecting sympathetic neurons and signaling via β2-adrenergic receptors (β2AR) on MMs. In contrast, helminth-mediated neuroprotectionwas dependent on T cells and systemic production of interleukin (IL)-4 and IL-13 byeosinophils, which induced arginase-expressing MMs that prevented neuronal loss froman unrelated infection located in a different intestinal region. Collectively, thesedata suggest that distinct enteric pathogens trigger a state of disease or tissuetolerance that preserves ENS number and functionality.
DOI: 10.1016/j.cell.2021.10.004
Source: https://www.cell.com/cell/fulltext/S0092-8674(21)01178-8