VBNC Cronobacter sakazakii survives in macrophages by resisting oxidative stress and evading recognition by macrophages.

IF 4 2区 生物学 Q2 MICROBIOLOGY
Yuanyuan Liu, Jingfeng Zhang, Haoqing Zhao, Feifeng Zhong, Jianyu Li, Lichao Zhao
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Abstract

Survival in host macrophages is an effective strategy for pathogenic bacterial transmission and pathogenesis. Our previous study found that viable but non-culturable (VBNC) Cronobacter Sakazakii (C. sakazakii) can survive in macrophages, but its survival mechanism is not clear. In this study, we investigated the possible mechanisms of VBNC C. sakazakii survival in macrophages in terms of environmental tolerance within macrophages and evasion of macrophages recognition. The results revealed that VBNC C. sakazakii survived under oxidative conditions at a higher rate than the culturable C. sakazakii. Moreover, the stringent response gene (relA and spoT) and the antioxidant-related genes (sodA, katG, and trxA) were up-regulated, indicating that VBNC C. sakazakii may regulate antioxidation through stringent response. On the other hand, compared with culturable C. sakazakii, VBNC C. sakazakii caused reduced response (Toll-like receptor 4) in macrophages, which was attributed to the suppression of biosynthesis of the lipopolysaccharides (LPS). Furthermore, we found that ellagic acid can reduce the survival rate of bacteria in macrophages by improving the immune TLR4 recognition ability of macrophages. In conclusion, VBNC C. sakazakii may survive in macrophages by regulating oxidative tolerance through stringent response and altering LPS synthesis to evade TLR4 recognition by macrophages, which suggests the pathogenic risk of VBNC C. sakazakii.

VBNC Cronobacter sakazakii通过抵抗氧化应激和逃避巨噬细胞的识别在巨噬细胞中存活。
在宿主巨噬细胞中存活是病原菌传播和致病的一种有效策略。我们之前的研究发现,可存活但不可培养(VBNC)的阪崎克罗诺杆菌(C. sakazakii)可在巨噬细胞中存活,但其存活机制尚不清楚。本研究从巨噬细胞内环境耐受性和逃避巨噬细胞识别两个方面研究了 VBNC C. sakazakii 在巨噬细胞中存活的可能机制。结果发现,在氧化条件下,VBNC C. sakazakii 的存活率高于可培养的 C. sakazakii。此外,严格响应基因(relA和spoT)和抗氧化相关基因(sodA、katG和trxA)上调,表明VBNC C. sakazakii可能通过严格响应调节抗氧化。另一方面,与可培养的 C. sakazakii 相比,VBNC C. sakazakii 在巨噬细胞中引起的反应(Toll 样受体 4)降低,这归因于脂多糖(LPS)的生物合成受到抑制。此外,我们还发现鞣花酸可以通过提高巨噬细胞的免疫 TLR4 识别能力来降低细菌在巨噬细胞中的存活率。总之,VBNC阪崎肠杆菌可能通过严格反应调节氧化耐受性,改变LPS合成以逃避巨噬细胞的TLR4识别,从而在巨噬细胞中存活,这提示了VBNC阪崎肠杆菌的致病风险。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
BMC Microbiology
BMC Microbiology 生物-微生物学
CiteScore
7.20
自引率
0.00%
发文量
280
审稿时长
3 months
期刊介绍: BMC Microbiology is an open access, peer-reviewed journal that considers articles on analytical and functional studies of prokaryotic and eukaryotic microorganisms, viruses and small parasites, as well as host and therapeutic responses to them and their interaction with the environment.
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