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首页> 外文期刊>Biochimica et biophysica acta. Biomembranes >S. Typhimurium strategies to resist killing by cationic antimicrobial peptides
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S. Typhimurium strategies to resist killing by cationic antimicrobial peptides

机译:S. Typhimurium策略抵抗阳离子抗菌肽杀伤

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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:S. Typhimurium是一种广泛的宿主范围革兰氏阴性病原体,必须逃避主体先天免疫系统杀害,以进行殖民,复制,导致疾病,并传送到其他主体。 Salmonellae的主要致病策略是真核细胞吞噬液泡中的入口,存活率和复制。这些吞噬液泡和胃肠粘膜表面含有多种阳离子抗菌肽(阵营),其控制入侵细菌。 S. Typhimurium拥有几种抵抗营地杀伤的关键机制,涉及传感阵营和膜损伤,以激活导致细菌包膜重塑的信号传导级联,以减少疏水性的增加,以降低营地的结合和有效性。此外,Salmonellae具有抵抗阵营的抗损伤的额外机制,包括靶向表面上的阳离子肽的外膜蛋白酶,以及保护内膜免受损伤的特定流出泵。本文是标题的特殊问题的一部分:对抗微生物肽的细菌抗性。 (c)2015 Elsevier B.v.保留所有权利。

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