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细菌肽聚糖作为慢性脑炎症的驱动因素。

Bacterial Peptidoglycan as a Driver of Chronic Brain Inflammation.

机构信息

Department of Biomedical Sciences of Cells and Systems, Section of Molecular Neurobiology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.

Department of Biomedical Sciences of Cells and Systems, Section of Molecular Neurobiology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands; Department of Anatomy and Neuroscience, Free University Amsterdam, Amsterdam, The Netherlands.

出版信息

Trends Mol Med. 2020 Jul;26(7):670-682. doi: 10.1016/j.molmed.2019.11.006. Epub 2020 Feb 21.

DOI:10.1016/j.molmed.2019.11.006
PMID:32589935
Abstract

Peptidoglycan (PGN) is a cell wall component of both Gram-positive and Gram-negative bacteria. Signature fragments of PGN are proinflammatory through engagement of pattern recognition receptors (PRR) on resident tissue cells and circulating leukocytes. Despite its abundance in the gut microbiota, there is limited recognition that PGN could contribute to chronic neuroinflammation. This review highlights current insights into the roles of PGN as a determinant of brain inflammation, notably in multiple sclerosis (MS) and its experimental autoimmune encephalomyelitis (EAE) models. Recent studies demonstrate PGN in blood of healthy adult humans. PGN amplifies autoimmune pathology via activation of innate immune cells. Novel uptake routes through (altered) gut mucosa by myeloid leukocyte subsets promote PGN transport to the brain.

摘要

肽聚糖(PGN)是革兰氏阳性菌和革兰氏阴性菌细胞壁的组成部分。PGN 的特征片段通过与驻留组织细胞和循环白细胞上的模式识别受体(PRR)结合而具有促炎作用。尽管它在肠道微生物群中大量存在,但人们对 PGN 可能导致慢性神经炎症的认识有限。这篇综述强调了 PGN 作为大脑炎症决定因素的作用的最新见解,特别是在多发性硬化症(MS)及其实验性自身免疫性脑脊髓炎(EAE)模型中。最近的研究表明,健康成年人体内存在 PGN。PGN 通过激活先天免疫细胞来放大自身免疫病理。髓样白细胞亚群通过(改变的)肠道黏膜的新摄取途径促进 PGN 向大脑的转运。

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