Abstract：
The bacterial flagellum is an elongated filament that protrudes from the cell and is responsible for bacterial motility. It can also be a pathogen-associated molecular pattern (PAMP) that regulates the host immune response and is involved in bacterial pathogenicity. In contrast to motile bacteria, the Brucella flagellum does not serve a motile purpose. Instead, it plays a role in regulating Brucella virulence and the host\'s immune response, similar to other non-motile bacteria. The flagellin protein, FliK, plays a key role in assembly of the flagellum and also as a potential virulence factor involved in the regulation of bacterial virulence and pathogenicity. In this study, we generated a Brucella suis S2 flik gene deletion strain and its complemented strain and found that deletion of the flik gene has no significant effect on the main biological properties of Brucella, but significantly enhanced the inflammatory response induced by Brucella infection of RAW264.7 macrophages. Further experiments demonstrated that the FliK protein was able to inhibit LPS-induced cellular inflammatory responses by down-regulating the expression of MyD88 and NF-κB, and by decreasing p65 phosphorylation in the NF-κB pathway; it also inhibited the expression of NLRP3 and caspase-1 in the NLRP3 inflammasome pathway. In conclusion, our study suggests that Brucella FliK may act as a virulence factor involved in the regulation of Brucella pathogenicity and modulation of the host immune response.
摘要：
细菌鞭毛是细长的细丝，从细胞突出并负责细菌运动。它也可以是调节宿主免疫应答并参与细菌致病性的病原体相关分子模式(PAMP)。与能动的细菌相反，布鲁氏菌鞭毛没有运动目的。相反，它在调节布鲁氏菌毒力和宿主的免疫反应中发挥作用，与其他非活动细菌相似。鞭毛蛋白，Flik,在鞭毛的组装中起着关键作用，也是参与细菌毒力和致病性调节的潜在毒力因子。在这项研究中,构建猪布鲁氏菌S2flk基因缺失株及其互补株,发现flk基因缺失对布鲁氏菌主要生物学特性无显著影响,但显著增强了布鲁氏菌感染RAW264.7巨噬细胞引起的炎症反应。进一步的实验表明，FliK蛋白能够通过下调MyD88和NF-κB的表达来抑制LPS诱导的细胞炎症反应，并通过减少NF-κB途径中的p65磷酸化；它还抑制NLRP3炎症小体途径中NLRP3和caspase-1的表达。总之,我们的研究表明，布鲁氏菌FliK可能是一种毒力因子，参与布鲁氏菌致病性的调节和宿主免疫反应的调节。
