Department of Microbiology and Cell Biology, Indian Institute of Science, Bangalore, India.
Centre for BioSystems Science and Engineering, Indian Institute of Science, Bangalore, India.
PLoS Pathog. 2022 Apr 28;18(4):e1010407. doi: 10.1371/journal.ppat.1010407. eCollection 2022 Apr.
Salmonella is a facultative intracellular pathogen that has co-evolved with its host and has also developed various strategies to evade the host immune responses. Salmonella recruits an array of virulence factors to escape from host defense mechanisms. Previously chitinase A (chiA) was found to be upregulated in intracellular Salmonella. Although studies show that several structurally similar chitinases and chitin-binding proteins (CBP) of many human pathogens have a profound role in various aspects of pathogenesis, like adhesion, virulence, and immune evasion, the role of chitinase in the intravacuolar pathogen Salmonella has not yet been elucidated. Therefore, we made chromosomal deletions of the chitinase encoding gene (chiA) to study the role of chitinase of Salmonella enterica in the pathogenesis of the serovars, Typhimurium, and Typhi using in vitro cell culture model and two different in vivo hosts. Our data indicate that ChiA removes the terminal sialic acid moiety from the host cell surface, and facilitates the invasion of the pathogen into the epithelial cells. Interestingly we found that the mutant bacteria also quit the Salmonella-containing vacuole and hyper-proliferate in the cytoplasm of the epithelial cells. Further, we found that ChiA aids in reactive nitrogen species (RNS) and reactive oxygen species (ROS) production in the phagocytes, leading to MHCII downregulation followed by suppression of antigen presentation and antibacterial responses. Notably, in the murine host, the mutant shows compromised virulence, leading to immune activation and pathogen clearance. In continuation of the study in C. elegans, Salmonella Typhi ChiA was found to facilitate bacterial attachment to the intestinal epithelium, intestinal colonization, and persistence by downregulating antimicrobial peptides. This study provides new insights on chitinase as an important and novel virulence determinant that helps in immune evasion and increased pathogenesis of Salmonella.
沙门氏菌是一种兼性细胞内病原体,与宿主共同进化,并发展了各种策略来逃避宿主的免疫反应。沙门氏菌招募了一系列毒力因子来逃避宿主的防御机制。先前发现,细胞内沙门氏菌中chiA(几丁质酶 A)上调。尽管研究表明,许多人类病原体中几种结构相似的几丁质酶和几丁质结合蛋白(CBP)在发病机制的各个方面都具有深远的作用,如粘附、毒力和免疫逃避,但几丁质酶在胞内病原体沙门氏菌中的作用尚未阐明。因此,我们通过体外细胞培养模型和两种不同的体内宿主,对chiA(几丁质酶编码基因)进行染色体缺失,以研究沙门氏菌血清型 Typhimurium 和 Typhi 中几丁质酶在发病机制中的作用。我们的数据表明,ChiA 从宿主细胞表面去除末端唾液酸部分,并促进病原体侵入上皮细胞。有趣的是,我们发现突变细菌也会离开沙门氏菌包含的空泡,并在上皮细胞的细胞质中过度增殖。此外,我们发现 ChiA 有助于吞噬细胞中活性氮(RNS)和活性氧(ROS)的产生,导致 MHCII 下调,随后抑制抗原呈递和抗菌反应。值得注意的是,在小鼠宿主中,突变体的毒力降低,导致免疫激活和病原体清除。在继续进行的秀丽隐杆线虫研究中,发现沙门氏菌 Typhi ChiA 通过下调抗菌肽来促进细菌附着到肠上皮细胞、肠道定植和持续存在。本研究为几丁质酶作为一种重要的新型毒力决定因素提供了新的见解,有助于沙门氏菌的免疫逃避和发病机制增强。