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AI-2/LuxS 群体感应系统在生物膜形成、.发病机制中的特征

Characterization of AI-2/LuxS quorum sensing system in biofilm formation, pathogenesis of .

机构信息

College of Veterinary Medicine, Northwest A&F University, Yangling, Shaanxi, China.

School of Life Science and Engineering, Foshan University, Foshan, China.

出版信息

Front Cell Infect Microbiol. 2024 Feb 6;14:1339131. doi: 10.3389/fcimb.2024.1339131. eCollection 2024.

DOI:10.3389/fcimb.2024.1339131
PMID:38379770
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10876813/
Abstract

(SEZ) is an opportunistic pathogen of both humans and animals. Quorum sensing (QS) plays an important role in the regulation of bacterial group behaviors. The aim of this study was to characterize the LuxS in SEZ and evaluate its impact on biofilm formation, pathogenesis and gene expression. The wild-type SEZ and its LuxS mutant (Δ) were examined for growth, biofilm formation, virulence factors, and transcriptomic profiles. Our results showed that LuxS deficiency did not affect SEZ hemolytic activity, adhesion or capsule production. For biofilm assay demonstrated that mutation in the gene significantly enhances biofilm formation, produced a denser biofilm and attached to a glass surface. RAW264.7 cell infection indicated that Δ promoted macrophage apoptosis and pro-inflammatory responses. In mice infection, there was no significant difference in mortality between SEZ and Δ. However, the bacterial load in the spleen of mice infected with Δ was significantly higher than in those infected with SEZ. And the pathological analysis further indicated that spleen damage was more severe in the Δ group. Moreover, transcriptomics analysis revealed significant alterations in carbon metabolism, RNA binding and stress response genes in Δ. In summary, this study provides the first evidence of AI-2/LuxS QS system in SEZ and reveals its regulatory effects on biofilm formation, pathogenicity and gene expression.

摘要

(SEZ) 是一种人类和动物的机会致病菌。群体感应 (QS) 在调节细菌群体行为方面起着重要作用。本研究旨在对 SEZ 中的 LuxS 进行表征,并评估其对生物膜形成、发病机制和基因表达的影响。野生型 SEZ 及其 LuxS 突变体 (Δ) 的生长、生物膜形成、毒力因子和转录组谱进行了研究。结果表明,LuxS 缺失不影响 SEZ 的溶血活性、黏附或荚膜生成。生物膜测定表明,基因的突变显著增强了生物膜的形成,产生了更密集的生物膜并附着在玻璃表面上。RAW264.7 细胞感染表明 Δ 促进了巨噬细胞凋亡和促炎反应。在小鼠感染中,SEZ 和 Δ 之间的死亡率没有显著差异。然而,感染 Δ 的小鼠脾脏中的细菌负荷明显高于感染 SEZ 的小鼠。病理分析进一步表明,Δ 组的脾脏损伤更严重。此外,转录组学分析显示,Δ 中碳代谢、RNA 结合和应激反应基因发生了显著改变。综上所述,本研究首次提供了 SEZ 中 AI-2/LuxS QS 系统的证据,并揭示了其对生物膜形成、致病性和基因表达的调节作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2239/10876813/b1890040f214/fcimb-14-1339131-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2239/10876813/710bbf543a27/fcimb-14-1339131-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2239/10876813/5ef2a75a1ed8/fcimb-14-1339131-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2239/10876813/8e3cb6b0cdb7/fcimb-14-1339131-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2239/10876813/ba180e04f179/fcimb-14-1339131-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2239/10876813/8bcd70d5eb13/fcimb-14-1339131-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2239/10876813/b1890040f214/fcimb-14-1339131-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2239/10876813/710bbf543a27/fcimb-14-1339131-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2239/10876813/2ee739e7f42d/fcimb-14-1339131-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2239/10876813/e0a6ef0c8e7b/fcimb-14-1339131-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2239/10876813/5ef2a75a1ed8/fcimb-14-1339131-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2239/10876813/8e3cb6b0cdb7/fcimb-14-1339131-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2239/10876813/ba180e04f179/fcimb-14-1339131-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2239/10876813/8bcd70d5eb13/fcimb-14-1339131-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2239/10876813/b1890040f214/fcimb-14-1339131-g008.jpg

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