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一种细菌色素介导的对先天免疫的跨物种保护。

Cross-Species Protection to Innate Immunity Mediated by A Bacterial Pigment.

作者信息

Liu Yiwei, McQuillen Eleanor A, Rana Pranav S J B, Gloag Erin S, Wozniak Daniel J

出版信息

bioRxiv. 2023 Jan 17:2023.01.15.524085. doi: 10.1101/2023.01.15.524085.

DOI:10.1101/2023.01.15.524085
PMID:36711503
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9882196/
Abstract

Bacterial infections are often polymicrobial. and cause chronic co-infections, which are more problematic than mono-species infections. We found that the production of membrane-bound pigment staphyloxanthin (STX), was induced by the exoproduct, 2-heptyl-4-hydroxyquinoline N-oxide (HQNO). The induction phenotype was conserved in and clinical isolates examined. When subjected to hydrogen peroxide or human neutrophils, survival was significantly higher when mixed with wild-type (WT) , compared to a mutant deficient in STX production or alone. In a murine wound model, co-infection with WT , but not the STX-deficient mutant, enhanced burden and disease compared to mono-infection. In conclusion, we discovered a novel role for HQNO mediating polymicrobial interactions with by inducing STX production, which consequently promotes resistance of both pathogens to innate immune effectors. These results further our understanding of how different bacterial species cooperatively cause co-infections.

摘要

细菌感染通常是多菌种的,并会引发慢性合并感染,这种感染比单一菌种感染更具问题。我们发现,膜结合色素葡萄球菌黄素(STX)的产生是由外产物2-庚基-4-羟基喹啉N-氧化物(HQNO)诱导的。在所检测的临床分离株中,诱导表型是保守的。当暴露于过氧化氢或人类中性粒细胞时,与STX产生缺陷的突变体或单独的相比,与野生型混合时的存活率显著更高。在小鼠伤口模型中,与野生型共同感染而非STX缺陷突变体,与单一感染相比,增加了负担和疾病。总之,我们发现HQNO通过诱导STX产生介导与的多菌种相互作用具有新作用,这进而促进了两种病原体对先天免疫效应物的抗性。这些结果进一步加深了我们对不同细菌物种如何协同导致合并感染的理解。