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血清载脂蛋白 A-I 增强溶葡球菌素 E 对金黄色葡萄球菌的治疗效果。

Serum apolipoprotein A-I potentiates the therapeutic efficacy of lysocin E against Staphylococcus aureus.

机构信息

Teikyo University Institute of Medical Mycology, Tokyo, Japan.

Division of Sport and Health Science, Graduate School of Medical Care and Technology, Teikyo University, Tokyo, Japan.

出版信息

Nat Commun. 2021 Nov 4;12(1):6364. doi: 10.1038/s41467-021-26702-0.

DOI:10.1038/s41467-021-26702-0
PMID:34737305
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8568920/
Abstract

Lysocin E is a lipopeptide with antibiotic activity against methicillin-resistant Staphylococcus aureus. For unclear reasons, the antibacterial activity of lysocin E in a mouse systemic infection model is higher than expected from in vitro results, and the in vitro activity is enhanced by addition of bovine serum. Here, we confirm that serum from various species, including humans, increases lysocin E antimicrobial activity, and identify apolipoprotein A-I (ApoA-I) as an enhancing factor. ApoA-I increases the antibacterial activity of lysocin E when added in vitro, and the antibiotic displays reduced activity in ApoA-I gene knockout mice. Binding of ApoA-I to lysocin E is enhanced by lipid II, a cell-wall synthesis precursor found in the bacterial membrane. Thus, the antimicrobial activity of lysocin E is potentiated through interactions with host serum proteins and microbial components.

摘要

赖氨酸素 E 是一种具有抗耐甲氧西林金黄色葡萄球菌活性的脂肽。由于原因不明,赖氨酸素 E 在小鼠全身感染模型中的抗菌活性高于体外结果预期,并且牛血清的添加增强了其体外活性。在这里,我们证实来自各种物种的血清,包括人类,增加了赖氨酸素 E 的抗菌活性,并确定载脂蛋白 A-I (ApoA-I) 为增强因子。ApoA-I 在体外添加时可增加赖氨酸素 E 的抗菌活性,并且抗生素在 ApoA-I 基因敲除小鼠中的活性降低。ApoA-I 与脂肽 II(一种存在于细菌膜中的细胞壁合成前体)结合可增强赖氨酸素 E 的抗菌活性。因此,赖氨酸素 E 的抗菌活性通过与宿主血清蛋白和微生物成分的相互作用得到增强。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/700b/8568920/dee77f9b2d96/41467_2021_26702_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/700b/8568920/9054505f139c/41467_2021_26702_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/700b/8568920/fabb6d706616/41467_2021_26702_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/700b/8568920/2ddc34393f48/41467_2021_26702_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/700b/8568920/dee77f9b2d96/41467_2021_26702_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/700b/8568920/9054505f139c/41467_2021_26702_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/700b/8568920/fabb6d706616/41467_2021_26702_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/700b/8568920/2ddc34393f48/41467_2021_26702_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/700b/8568920/dee77f9b2d96/41467_2021_26702_Fig4_HTML.jpg

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