Matamouros Susana, Miller Samuel I
Departments of Microbiology, University of Washington, Seattle, WA 98195, USA.
Departments of Microbiology, University of Washington, Seattle, WA 98195, USA; Departments of Genome Sciences, University of Washington, Seattle, WA 98195, USA; Department of Medicine, University of Washington, Seattle, WA 98195, USA.
Biochim Biophys Acta. 2015 Nov;1848(11 Pt B):3021-5. doi: 10.1016/j.bbamem.2015.01.013. Epub 2015 Jan 30.
S. Typhimurium is a broad host range Gram-negative pathogen that must evade killing by host innate immune systems to colonize, replicate, cause disease, and be transmitted to other hosts. A major pathogenic strategy of Salmonellae is entrance, survival, and replication within eukaryotic cell phagocytic vacuoles. These phagocytic vacuoles and gastrointestinal mucosal surfaces contain multiple cationic antimicrobial peptides (CAMPs) which control invading bacteria. S. Typhimurium possesses several key mechanisms to resist killing by CAMPs which involve sensing CAMPs and membrane damage to activate signaling cascades that result in remodeling of the bacterial envelope to reduce its overall negative charge with an increase in hydrophobicity to decrease binding and effectiveness of CAMPs. Moreover Salmonellae have additional mechanisms to resist killing by CAMPs including an outer membrane protease which targets cationic peptides at the surface, and specific efflux pumps which protect the inner membrane from damage. This article is part of a Special Issue entitled: Bacterial Resistance to Antimicrobial Peptides.
鼠伤寒沙门氏菌是一种宿主范围广泛的革兰氏阴性病原体,它必须逃避宿主先天免疫系统的杀伤才能进行定植、复制、致病并传播给其他宿主。沙门氏菌的主要致病策略是进入、存活于真核细胞吞噬泡内并在其中复制。这些吞噬泡和胃肠道黏膜表面含有多种控制入侵细菌的阳离子抗菌肽(CAMP)。鼠伤寒沙门氏菌拥有多种关键机制来抵抗CAMP的杀伤,这涉及感知CAMP和膜损伤以激活信号级联反应,从而导致细菌包膜重塑,降低其总体负电荷并增加疏水性,以减少CAMP的结合和有效性。此外,沙门氏菌还有其他抵抗CAMP杀伤的机制,包括一种靶向表面阳离子肽的外膜蛋白酶,以及保护内膜免受损伤的特定外排泵。本文是名为“细菌对抗菌肽的抗性”的特刊的一部分。