Abstract
Salmonella Typhimurium is a common pathogen infecting the gastrointestinal tract of humans and animals, causing host gastroenteritis and typhoid fever. Heat shock protein (HtpG) as a molecular chaperone is involved in the various cellular processes of bacteria, especially under environmental stress. However, the potential association of HtpG with S. Typhimurium infection remains unknown. In this study, we clarified that HtpG could also play a role as an effector in S. Typhimurium infection. RNA-seq indicated that the flagellar assembly pathway, infection pathway, and chemotaxis pathway genes of S. Typhimurium were downregulated after the mutation of HtpG, which resulted in compromises of S. Typhimurium motility, biofilm formation, adhesion, invasion, and inflammation-inducing ability. In addition, HtpG recombinant protein was capable of promoting the proliferation of S. Typhimurium in host cells and the resultant inflammation. Collectively, our results illustrated an important role of HtpG in S. Typhimurium infection.
Highlights
The results of qPCR showed that the relative expression of HtpG mRNA in mutant strains was significantly reduced (p < 0.01), while that of supplemented strains was significantly increased (p < 0.01) (Figure 1)
The results showed that the diameter of the swimming circle of DhtpG strains was significantly smaller than that of wild type (WT) strains and CDhtpG strains (p < 0.05) (Figure 3A)
The results showed that the amount of biofilm formed by the DhtpG strains was significantly lower than that of the WT strains and CDhtpG strains (p < 0.05)
Summary
S. Typhimurium is a Gram-negative bacterium from Enterobacteriaceae, which can colonize the intestine of humans and a variety of animals (e.g., pigs, chickens, and cattle), causing gastroenteritis (Majowicz et al, 2010). Salmonella can be directly swallowed by dendritic cells (DCs) in the lamina propria (LP) of the small intestine epithelium (Tam et al, 2008). Salmonella can survive in DCs or macrophages in PP or LP, and rapidly spread through the reticuloendothelial cell system and colonize the liver and spleen (Haraga et al, 2008), followed by spread throughout the body through the blood, causing various symptoms such as diarrhea, vomiting, fever, and abdominal pain (LaRock et al, 2015).
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