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表皮葡萄球菌通过体外释放细胞外 DNA 改变巨噬细胞极化和吞噬作用。

Staphylococcus epidermidis alters macrophage polarization and phagocytic uptake by extracellular DNA release in vitro.

机构信息

Institut für Medizinische Mikrobiologie, Virologie und Hygiene, Universitätsklinikum Hamburg-Eppendorf (UKE), Hamburg, Germany.

UKE Microscopy Imaging Facility (Umif), Universitätsklinikum Hamburg-Eppendorf (UKE), Hamburg, Germany.

出版信息

NPJ Biofilms Microbiomes. 2024 Nov 20;10(1):131. doi: 10.1038/s41522-024-00604-7.

DOI:10.1038/s41522-024-00604-7
PMID:39567551
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11579364/
Abstract

Biofilm formation shields Staphylococcus epidermidis from host defense mechanisms, contributing to chronic implant infections. Using wild-type S. epidermidis 1457, a PIA-negative mutant (1457-M10), and an eDNA-negative mutant (1457ΔatlE), this study examined the influence of biofilm matrix components on human monocyte-derived macrophage (hMDM) interactions. The wild-type strain was resistant to phagocytosis and induced an anti-inflammatory response in hMDMs, while both mutants were more susceptible to phagocytosis and triggered a pro-inflammatory response. Removing eDNA from the 1457 biofilm matrix increased hMDM uptake and a pro-inflammatory reaction, whereas adding eDNA to the 1457ΔatlE mutant reduced phagocytosis and promoted an anti-inflammatory response. Inhibiting TLR9 enhanced bacterial uptake and induced a pro-inflammatory response in hMDMs exposed to wild-type S. epidermidis. This study highlights the critical role of eDNA in immune evasion and the central role of TLR9 in modulating macrophage responses, advancing the understanding of implant infections.

摘要

生物膜的形成使表皮葡萄球菌免受宿主防御机制的影响，导致慢性植入物感染。本研究使用野生型表皮葡萄球菌 1457、PIA 阴性突变体（1457-M10）和 eDNA 阴性突变体（1457ΔatlE），研究了生物膜基质成分对人单核细胞衍生的巨噬细胞（hMDM）相互作用的影响。野生型菌株对吞噬作用具有抗性，并在 hMDM 中诱导抗炎反应，而两种突变体更容易被吞噬作用触发促炎反应。从 1457 生物膜基质中去除 eDNA 增加了 hMDM 的摄取和促炎反应，而向 1457ΔatlE 突变体中添加 eDNA 则减少了吞噬作用并促进了抗炎反应。抑制 TLR9 增强了暴露于野生型表皮葡萄球菌的 hMDM 的细菌摄取并诱导促炎反应。本研究强调了 eDNA 在免疫逃逸中的关键作用以及 TLR9 在调节巨噬细胞反应中的核心作用，推进了对植入物感染的理解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4472/11579364/0d5a719b027d/41522_2024_604_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4472/11579364/a7669ce978a3/41522_2024_604_Fig1_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4472/11579364/7fc4a70b5656/41522_2024_604_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4472/11579364/0d5a719b027d/41522_2024_604_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4472/11579364/a7669ce978a3/41522_2024_604_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4472/11579364/202ffd3c0629/41522_2024_604_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4472/11579364/187e4d6236b9/41522_2024_604_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4472/11579364/c74efc7d4a35/41522_2024_604_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4472/11579364/9b7d591d5bc5/41522_2024_604_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4472/11579364/7fc4a70b5656/41522_2024_604_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4472/11579364/0d5a719b027d/41522_2024_604_Fig7_HTML.jpg

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J Innate Immun. 2023;15(1):499-515. doi: 10.1159/000530385. Epub 2023 Apr 3.
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