A ROD9 island encoded gene in Salmonella Enteritidis plays an important role in acid tolerance response and helps in systemic infection in mice

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. En...

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Autores principales: Susmita Das, Shilpa Ray, Aryashree Arunima, Bikash Sahu, Mrutyunjay Suar
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Publicado: Taylor & Francis Group 2020
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spelling oai:doaj.org-article:978a244e9ec54fe3a1e2812e367c3df72021-11-17T14:21:58ZA ROD9 island encoded gene in Salmonella Enteritidis plays an important role in acid tolerance response and helps in systemic infection in mice2150-55942150-560810.1080/21505594.2020.1733203https://doaj.org/article/978a244e9ec54fe3a1e2812e367c3df72020-12-01T00:00:00Zhttp://dx.doi.org/10.1080/21505594.2020.1733203https://doaj.org/toc/2150-5594https://doaj.org/toc/2150-5608Salmonella, 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 ΔSEN1008 failed to survive during ATR assay, indicating its role under acid stress. Together, our findings suggested ΔSEN1008 to be significantly attenuated and we propose this gene to be a potent factor responsible for S. Enteritidis pathogenesis.Susmita DasShilpa RayAryashree ArunimaBikash SahuMrutyunjay SuarTaylor & Francis Grouparticlesalmonella enteritidisrod9sen1008acid tolerancec57bl/6inflammationInfectious and parasitic diseasesRC109-216ENVirulence, Vol 11, Iss 1, Pp 247-259 (2020)
institution DOAJ
collection DOAJ
language EN
topic salmonella enteritidis
rod9
sen1008
acid tolerance
c57bl/6
inflammation
Infectious and parasitic diseases
RC109-216
spellingShingle salmonella enteritidis
rod9
sen1008
acid tolerance
c57bl/6
inflammation
Infectious and parasitic diseases
RC109-216
Susmita Das
Shilpa Ray
Aryashree Arunima
Bikash Sahu
Mrutyunjay Suar
A ROD9 island encoded gene in Salmonella Enteritidis plays an important role in acid tolerance response and helps in systemic infection in mice
description 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 ΔSEN1008 failed to survive during ATR assay, indicating its role under acid stress. Together, our findings suggested ΔSEN1008 to be significantly attenuated and we propose this gene to be a potent factor responsible for S. Enteritidis pathogenesis.
format article
author Susmita Das
Shilpa Ray
Aryashree Arunima
Bikash Sahu
Mrutyunjay Suar
author_facet Susmita Das
Shilpa Ray
Aryashree Arunima
Bikash Sahu
Mrutyunjay Suar
author_sort Susmita Das
title A ROD9 island encoded gene in Salmonella Enteritidis plays an important role in acid tolerance response and helps in systemic infection in mice
title_short A ROD9 island encoded gene in Salmonella Enteritidis plays an important role in acid tolerance response and helps in systemic infection in mice
title_full A ROD9 island encoded gene in Salmonella Enteritidis plays an important role in acid tolerance response and helps in systemic infection in mice
title_fullStr A ROD9 island encoded gene in Salmonella Enteritidis plays an important role in acid tolerance response and helps in systemic infection in mice
title_full_unstemmed A ROD9 island encoded gene in Salmonella Enteritidis plays an important role in acid tolerance response and helps in systemic infection in mice
title_sort rod9 island encoded gene in salmonella enteritidis plays an important role in acid tolerance response and helps in systemic infection in mice
publisher Taylor & Francis Group
publishDate 2020
url https://doaj.org/article/978a244e9ec54fe3a1e2812e367c3df7
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