The Gall of Some Bacteria: Strange Behavior by Salmonella

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Science Translational Medicine  21 Mar 2012:
Vol. 4, Issue 126, pp. 126ec49
DOI: 10.1126/scitranslmed.3004012

Certain types of the bacterium Salmonella enterica can cause infections in humans, such as typhoid fever (Typhi), with the gallbladder being a common location of infection and dissemination. Antunes and colleagues report that bile—which is regulated by the gallbladder—may actually repress virulence to allow survival of Salmonella in a nonpathogenic “carrier state” in which bacteria peacefully coexist in humans, patiently waiting for their next virulent opportunity.

Using DNA microarrays, the authors found that various Salmonella Typhimurium metabolism-related genes were affected by bile. In particular, bile acted on the gene phoP, which is known to regulate virulence. The specific components of bile that stimulate phoP repression are not yet clear, but the major constituents of bile—bile acids—did not affect phoP signaling or sensing. Another curious result was the finding that commercial bovine bile (used in many studies as a human bile surrogate) did not repress phoP; pure bovine or murine bile were needed. This may help explain some conflicting reports on Salmonella growth and virulence in the gallbladder.

Nonvirulent behavior is not atypical for pathogenic bacteria. This was supported by Antunes et al., in which a known virulence gene was repressed in the rich growth conditions of bile. To develop new therapeutic strategies for diseases such as typhoid fever, we need to understand how pathogenic microbes, such as Salmonella, interpret and control their responses to their local environment. We have a poor understanding of “dormant” pathogen behavior in the body. However, determining how bacterial pathogens evade host defenses through avirulent behavior will aid in the development of better treatments for infected individuals and in attempts to limit bacterial disease transmission.

L. C. M. Antunes et al., Repression of Salmonella phoP expression by small molecules from physiological bile. J. Bacteriol. 24 February 2012 (10.1128/JB.00104-12). [Abstract]

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