A ROD9 island encoded gene in Salmonella Enteritidis plays an important role in acid tolerance response and helps in systemic infection in mice. Issue 1 (1st January 2020)

• Record Type: Journal Article
• Authors: Das, Susmita; Ray, Shilpa; Arunima, Aryashree; Sahu, Bikash; Suar, Mrutyunjay
• Is Part Of: Virulence. Volume 11:Issue 1(2020)
• Page Start: 247
• Page End: 259
• Publication Date: 2020-01-01
• Subjects: Salmonella Enteritidis -- ROD9 -- SEN1008 -- acid tolerance -- C57Bl/6 -- inflammation; Virulence (Microbiology) -- Periodicals; Bacterial diseases -- Periodicals; Molecular microbiology -- Periodicals; 579.05
• DOI: 10.1080/21505594.2020.1733203
• Languages: English
• ISSNs: 2150-5608

Abstract

ABSTRACT: Salmonella, like other pathogenic bacteria has undergone multiple genomic alterations to adapt itself into specific host environments executing varied degrees of virulence through evolution. Such variations in genome content have been assumed to lead the closely related non-typhoidal serovars, S . Enteritidis, and S . Typhimurium to exhibit Type Three Secretion System −2 (T3SS-2) based diverse colonization and inflammation kinetics. Mutually exclusive genes present in either of the serovars are recently being studied and in our currentwork, we focused on a particular island ROD9, present in S . Enteritidis but not in S . Typhimurium. Earlier reports have identified a few genes from this island to be responsible for virulence in vitro as well as in vivo . In this study, we have identified another gene, SEN1008 from the same island encoding a hypothetical protein to be a potential virulence determinant showing systemic attenuation upon mutation in C57BL/6 mice infection model. The isogenic mutant strain displayed reduced adhesion to epithelial cells in vitro as well as was highly immotile. It was also deficient in intracellular replication in vitro, with a highly suppressed SPI-2and failed to cause acute colitis at 72-h p.i. in vivo . Moreover, on acid exposure, SEN1008 showed 17 folds and 2 fold up-regulations during adaptation and challenge phases, respectively and Δ SEN1008 failed to survive during ATR assay, indicating its role under acid stress. Together, our findings suggested Δ SEN1008 to be significantly attenuated and we propose this gene to be a potent factor responsible for S . Enteritidis pathogenesis.