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S. Typhimurium strategies to resist killing by cationic antimicrobial peptides

机译:鼠伤寒沙门氏菌抵抗阳离子抗菌肽杀伤的策略

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摘要

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. (C) 2015 Elsevier B.V. All rights reserved.
机译:鼠伤寒沙门氏菌是一种广泛的宿主革兰氏阴性病原体,必须逃避宿主先天免疫系统的杀伤才能定殖,复制,引起疾病并传播给其他宿主。沙门氏菌的主要致病策略是真核细胞吞噬液泡内的进入,存活和复制。这些吞噬液泡和胃肠道粘膜表面含有多个控制入侵细菌的阳离子抗菌肽(CAMP)。鼠伤寒沙门氏菌具有几种抗CAMP杀伤的关键机制,包括感测CAMP和膜损伤以激活信号级联反应,从而导致细菌包膜重塑,从而降低其总体负电荷,并增加疏水性,从而降低CAMP的结合力和有效性。此外,沙门氏菌还具有抵抗CAMP杀伤的其他机制,包括在表面靶向阳离子肽的外膜蛋白酶和保护内膜不受损伤的特定外排泵。本文是名为“细菌对抗菌肽的耐药性”的特刊的一部分。 (C)2015 Elsevier B.V.保留所有权利。

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