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PLoS One. 2016 Jun 3;11(6):e0156932. doi: 10.1371/journal.pone.0156932. eCollection 2016.

Campylobacter jejuni CsrA Regulates Metabolic and Virulence Associated Proteins and Is Necessary for Mouse Colonization.

Author information

1
Department of Medicine, Division of Infectious Diseases, Augusta University, Augusta, GA, 30912, United States of America.
2
Department of Natural Sciences, Georgia Military College - Augusta, Augusta, GA, 30907, United States of America.
3
Department of Microbiology, University of Texas Southwestern Medical Center, Dallas, TX, 75390, United States of America.

Abstract

Campylobacter jejuni infection is a leading bacterial cause of gastroenteritis and a common antecedent leading to Gullian-Barré syndrome. Our previous data suggested that the RNA-binding protein CsrA plays an important role in regulating several important phenotypes including motility, biofilm formation, and oxidative stress resistance. In this study, we compared the proteomes of wild type, csrA mutant, and complemented csrA mutant C. jejuni strains in an effort to elucidate the mechanisms by which CsrA affects virulence phenotypes. The putative CsrA regulon was more pronounced at stationary phase (111 regulated proteins) than at mid-log phase (25 regulated proteins). Proteins displaying altered expression in the csrA mutant included diverse metabolic functions, with roles in amino acid metabolism, TCA cycle, acetate metabolism, and various other cell processes, as well as pathogenesis-associated characteristics such as motility, chemotaxis, oxidative stress resistance, and fibronectin binding. The csrA mutant strain also showed altered autoagglutination kinetics when compared to the wild type. CsrA specifically bound the 5' end of flaA mRNA, and we demonstrated that CsrA is a growth-phase dependent repressor of FlaA expression. Finally, the csrA mutant exhibited reduced ability to colonize in a mouse model when in competition with the wild type, further underscoring the role of CsrA in C. jejuni colonization and pathogenesis.

PMID:
27257952
PMCID:
PMC4892619
DOI:
10.1371/journal.pone.0156932
[Indexed for MEDLINE]
Free PMC Article

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