Vibrio cholerae VC1741 (PsrA) enhances the colonization of the pathogen in infant mice intestines in the presence of the long-chain fatty acid, oleic acid. (October 2020)

• Record Type: Journal Article
• Authors: Yang, Shuang; Xi, Daoyi; Wang, Xiaochen; Li, Yuehua; Li, Yujia; Yan, Junxiang; Cao, Boyang
• Is Part Of: Microbial pathogenesis. Volume 147(2020)
• Publication Date: 2020-10
• Subjects: Vibrio cholerae -- vc1741 -- Fatty acid degradation -- β-oxidation -- Intestinal colonization; CI competitive index -- cAMP cyclic 3′ 5′-AMP -- cyaA adenylate cyclase -- LCFA long-chain fatty acid -- WT wild-type -- LB Luria-Bertani -- qRT-PCR Quantitative Real-Time Polymerase Chain Reaction -- EMSA Electrophoretic Mobility Shift Assay -- MBP Maltose-binding protein -- acyl-CoA acyl coenzyme; Pathogenic microorganisms -- Periodicals; Pathology, Molecular -- Periodicals; Communicable Diseases -- microbiology -- Periodicals; Communicable Diseases -- parasitology -- Periodicals; Micro-organismes pathogènes -- Périodiques; Pathologie moléculaire -- Périodiques; Electronic journals; 616.9041
• DOI: 10.1016/j.micpath.2020.104443
• Languages: English
• ISSNs: 0882-4010

Abstract

Abstract: Vibrio cholerae is a natural inhabitant of aquatic environments and causes the epidemic diarrheal disease known as cholera. Fatty acid metabolism is closely related to the pathogenicity of V. cholerae . The TetR family transcriptional repressor PsrA regulates the β-oxidation pathway in Pseudomonas aeruginosa ; however, little is known about its regulation in V. cholerae . In this study, qRT-PCR revealed that the expression of vc1741 ( psrA ) increased 40-fold in the small intestines of infant mice compared with that grown in LB medium. The Δ vc1741 mutant showed a significant defected in the ability to colonize the small intestines of infant mice with a competitive index (CI) of 0.53. EMSAs indicated that VC1741 could directly bind to the promoter regions of vc1741 - fadE1, fadBA, and fadIJ operons, and these bindings were reversed upon addition of the long-chain fatty acid (LCFA), oleic acid. The expression levels of the fadB, fadA, fadI, and fadJ genes were all elevated by approximately 2-fold in the Δ vc1741 mutant strain compared with that in the wild-type strain in LB medium, indicating that VC1741 is a repressor for these genes involved in fatty acid degradation. Moreover, Δ fadBA, Δ fadB, and Δ fadA isogenic mutants showed defective abilities to colonize the small intestines of infant mice, with CI values of 0.64, 0.73, and 0.74, respectively. These data provided a mechanistic model in which LCFAs affect the expression of VC1741 to control fatty acid degradation and virulence in V. cholerae . Highlights: The Δ vc1741 mutant attenuates the ability of intestinal colonization compared with the wild-type strain. The vc1741 is directly repressed by the cAMP-CRP complex. VC1741 responds to long-chain fatty acid signal to regulate vc1741 - fadE1, fadBA, and fadIJ of the β-oxidation operons. Inactivation of fadB and fadA strains of V. cholerae E12382 attenuate the ability of infant mice intestinal colonization.