摘要：

The type-III secretion system-I (T3SS-I) of Salmonella enterica serovar Typhimurium (S. Typhimurium) is an essential component to mediate active invasion and subsequent inflammation in genetically susceptible C57BL/6 mice. S. Typhimurium translocates its effector proteins through Salmonella Pathogenicity Island-I (SPI-I) encoded T3SS-I needle complex. This study focuses on invH gene of S. Typhimurium, which plays an active role in SPI-I mediated effector protein translocation. The deletion of invH gene in S. Typhimurium reduced the invasion efficiency of the bacterium to 70–80% as compared to wild-type S. Typhimurium (SB300) in vitro. To further investigate the role of invH gene exclusively in SPI-1 mediated inflammation, C57BL/6 mice were infected with S. Typhimurium double mutant deficient in invH and ssaV. Results indicated significant difference in the degree of cecal inflammation between wild-type S. Typhimurium and double mutant at 12 h and 48 h post infection. However this difference was found to be more prominent at 12 h p.i. In line with our findings, analysis of effector protein secretion in invH, ssaV double mutant showed reduced secretion of Sip effector proteins (SipA, SipB, SipC and SipD) as compared to the wild-type strain. The inflammation phenotype was restored on complementing invH to its respective double mutant strain. Altogether, the current study proposes a possible role of invH gene in early cecal inflammation by Salmonella Typhimurium in mice colitis model.

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