Pathogenicity island excision during an infection by Salmonella enterica serovar Enteritidis is required for crossing the intestinal epithelial barrier in mice to cause systemic infection.

Bibliographic Details
Title: Pathogenicity island excision during an infection by Salmonella enterica serovar Enteritidis is required for crossing the intestinal epithelial barrier in mice to cause systemic infection.
Authors: Catalina Pardo-Roa, Geraldyne A Salazar, Loreani P Noguera, Francisco J Salazar-Echegarai, Omar P Vallejos, Isidora D Suazo, Bárbara M Schultz, Irenice Coronado-Arrázola, Alexis M Kalergis, Susan M Bueno
Source: PLoS Pathogens, Vol 15, Iss 12, p e1008152 (2019)
Publisher Information: Public Library of Science (PLoS), 2019.
Publication Year: 2019
Collection: LCC:Immunologic diseases. Allergy
LCC:Biology (General)
Subject Terms: Immunologic diseases. Allergy, RC581-607, Biology (General), QH301-705.5
More Details: Pathogenicity island excision is a phenomenon that occurs in several Salmonella enterica serovars and other members of the family Enterobacteriaceae. ROD21 is an excisable pathogenicity island found in the chromosome of S. Enteritidis, S. Dublin and S. Typhi among others, which contain several genes encoding virulence-associated proteins. Excision of ROD21 may play a role in the ability of S. Enteritidis to cause a systemic infection in mice. Our previous studies have shown that Salmonella strains unable to excise ROD21 display a reduced ability to colonize the liver and spleen. In this work, we determined the kinetics of ROD21 excision in vivo in C57BL/6 mice and its effect on virulence. We quantified bacterial burden and excision frequency in different portions of the digestive tract and internal organs throughout the infection. We observed that the frequency of ROD21 excision was significantly increased in the bacterial population colonizing mesenteric lymph nodes at early stages of the infective cycle, before 48 hours post-infection. In contrast, excision frequency remained very low in the liver and spleen at these stages. Interestingly, excision increased drastically after 48 h post infection, when intestinal re-infection and mortality begun. Moreover, we observed that the inability to excise ROD21 had a negative effect on S. Enteritidis capacity to translocate from the intestine to deeper organs, which correlates with an abnormal transcription of invA in the S. Enteritidis strain unable to excise ROD21. These results suggest that excision of ROD21 is a genetic mechanism required by S. Enteritidis to produce a successful invasion of the intestinal epithelium, a step required to generate systemic infection in mice.
Document Type: article
File Description: electronic resource
Language: English
ISSN: 1553-7366
1553-7374
Relation: https://journals.plos.org/plospathogens/article/file?id=10.1371/journal.ppat.1008152&type=printable; https://doaj.org/toc/1553-7366; https://doaj.org/toc/1553-7374
DOI: 10.1371/journal.ppat.1008152&type=printable
DOI: 10.1371/journal.ppat.1008152
Access URL: https://doaj.org/article/c743a75adb1c4755b926131c0ad7008a
Accession Number: edsdoj.743a75adb1c4755b926131c0ad7008a
Database: Directory of Open Access Journals
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More Details
ISSN:15537366
15537374
DOI:10.1371/journal.ppat.1008152&type=printable
Published in:PLoS Pathogens
Language:English