Fatty Acid Homeostasis Tunes Flagellar Motility by Activating Phase 2 Flagellin Expression, Contributing to Salmonella Gut Colonization
Fatty Acid Homeostasis Tunes Flagellar Motility by Activating Phase 2 Flagellin Expression, Contributing to Salmonella Gut Colonization
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DOI：
10.1128/iai.00184-22
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发表时间：
2022-06
影响因子：
3.1
通讯作者：
Y. Hoshino;Taro Sakamoto;Naoki Sudo;Masahiro Ito;Takeshi Haneda;N. Okada;T. Miki
中科院分区：
文献类型：
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作者：
Y. Hoshino;Taro Sakamoto;Naoki Sudo;Masahiro Ito;Takeshi Haneda;N. Okada;T. Miki
长链脂肪酸（LCFA）代谢是细菌中的一个基本细胞过程，涉及脂质稳态、能量产生和感染。然而，LCFA代谢在鼠伤寒沙门氏菌（S.摘要长链脂肪酸（LCFA）代谢是细菌中一个基本的细胞过程，参与脂质稳态、能量产生和感染。然而，LCFA代谢在鼠伤寒沙门氏菌（S. Tm）肠道感染仍不清楚。在这里，我们使用小鼠胃肠炎感染模型，证明了LCFA代谢参与S。我的肠道殖民化。LCFA代谢相关的转录调节因子FadR有助于S.我的肠道殖民化。fadR缺失改变了基因表达谱，导致鞭毛运动异常。TM. fadR突变体中的定殖缺陷可归因于改变的游泳行为，其特征在于不太频繁的平滑游泳，这是由2期鞭毛蛋白FljB的表达减少引起的。值得注意的是，fadR缺失导致脂质LCFA组成的变化导致fljB表达减少，其通过外源LCFA恢复。因此，LCFA稳态可能通过激活fljB表达来维持适当的鞭毛运动，从而促进S.我的肠道殖民化。我们的研究结果提高了对管腔LCFA对肠道病原体毒力影响的理解。
Long-chain-fatty-acid (LCFA) metabolism is a fundamental cellular process in bacteria that is involved in lipid homeostasis, energy production, and infection. However, the role of LCFA metabolism in Salmonella enterica serovar Typhimurium (S. ABSTRACT Long-chain-fatty-acid (LCFA) metabolism is a fundamental cellular process in bacteria that is involved in lipid homeostasis, energy production, and infection. However, the role of LCFA metabolism in Salmonella enterica serovar Typhimurium (S. Tm) gut infection remains unclear. Here, using a murine gastroenteritis infection model, we demonstrate involvement of LCFA metabolism in S. Tm gut colonization. The LCFA metabolism-associated transcriptional regulator FadR contributes to S. Tm gut colonization. fadR deletion alters the gene expression profile and leads to aberrant flagellar motility of S. Tm. Colonization defects in the fadR mutant are attributable to altered swimming behavior characterized by less frequently smooth swimming, resulting from reduced expression of the phase 2 flagellin FljB. Notably, changes in lipid LCFA composition by fadR deletion lead to reduced expression of fljB, which is restored by exogenous LCFA. Therefore, LCFA homeostasis may maintain proper flagellar motility by activating fljB expression, contributing to S. Tm gut colonization. Our findings improve the understanding of the effect of luminal LCFA on the virulence of enteric pathogens.