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Laboratory Techniques Used to Maintain and Differentiate Biotypes of Vibrio cholerae Clinical and Environmental Isolates
Published on: May 30, 2017
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The Vibrio cholerae VprA-VprB two-component system controls virulence through endotoxin modification
Carmen M Herrera1, Alexander A Crofts1, Jeremy C Henderson1
1Department of Molecular Biosciences, The University of Texas at Austin, Austin, Texas, USA.
Mbio
|December 25, 2014
Summary
Vibrio cholerae modifies its surface lipopolysaccharide (LPS) with glycine, evading immune peptides. A novel VprAB system regulates this, crucial for bacterial colonization and cholera pathogenesis.
Area of Science:
- Microbiology
- Infectious Diseases
- Bacterial Pathogenesis
Background:
- Vibrio cholerae causes cholera and exhibits resistance to cationic antimicrobial peptides (CAMPs).
- CAMP resistance in V. cholerae El Tor biotype is linked to glycine modification of lipopolysaccharide (LPS) lipid A.
- The regulatory mechanisms governing LPS modification in V. cholerae remain largely unknown.
Purpose of the Study:
- To identify the regulatory system controlling lipid A glycine modification in Vibrio cholerae.
- To investigate the role of this regulatory system in bacterial resistance to CAMPs and host colonization.
Main Methods:
- Identification and characterization of a novel two-component system (VprAB).
- Analysis of gene expression for the almEFG operon involved in lipid A modification.
- Assessment of bacterial survival in the presence of CAMPs and *in vivo* colonization studies.
Main Results:
- The VprAB two-component system regulates the expression of genes essential for glycine modification of LPS lipid A.
- VprAB-dependent lipid A modification confers resistance to polymyxin B, a CAMP.
- Both VprAB and the lipid A modification machinery are essential for V. cholerae colonization of the mammalian host.
Conclusions:
- A novel regulatory network involving the VprAB system controls LPS modification in V. cholerae.
- This mechanism enhances bacterial fitness by conferring resistance to host immune defenses.
- The identified pathway is critical for Vibrio cholerae pathogenesis and colonization.
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