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在全身性大肠杆菌感染的缺陷型抗菌肽缺乏小鼠模型中,腹膜巨噬细胞受损。

Peritoneal macrophages are impaired in cathelicidin-deficient mice systemically challenged with Escherichia coli.

机构信息

Cumming School of Medicine, University of Calgary, Calgary, Canada.

Microbiology, Immunology and Infectious Diseases, Cumming School of Medicine, University of Calgary, Calgary, Canada.

出版信息

Cell Tissue Res. 2021 Mar;383(3):1203-1208. doi: 10.1007/s00441-020-03362-y. Epub 2021 Jan 26.

Abstract

Cathelicidins are small, cationic peptides produced by macrophages with protective effects against infection although their involvement in phagocytosis is not fully understood. This study demonstrates that fewer macrophages were recruited in mice genetically deficient in cathelicidin (Camp) during acute Escherichia coli-induced peritonitis and those macrophages had impaired phagocytosis. These defects seem due to endogenous functions of murine cathelicidin (CRAMP) as phagocytosis was not improved by synthetic human cathelicidin (LL-37) in a murine phagocytic cell line. This knowledge contributes to understanding the function of cathelicidins in the recruitment and function of phagocytic cells and differential roles between endogenous and exogenous cathelicidins.

摘要

杀菌肽是由巨噬细胞产生的具有保护作用的小阳离子肽,尽管它们在吞噬作用中的作用尚未完全阐明。本研究表明,在急性大肠杆菌诱导的腹膜炎中,缺乏杀菌肽(Camp)基因的小鼠中募集的巨噬细胞较少,并且这些巨噬细胞的吞噬作用受损。这些缺陷似乎是由于鼠源杀菌肽(CRAMP)的内源性功能所致,因为在鼠源吞噬细胞系中,合成的人杀菌肽(LL-37)并不能改善吞噬作用。这一认识有助于理解杀菌肽在吞噬细胞募集和功能中的作用,以及内源性和外源性杀菌肽之间的差异作用。

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