作者: Kourtney P. Nickerson , Rachael B. Chanin , Jeticia R. Sistrunk , David A. Rasko , Peter J. Fink
DOI: 10.1128/IAI.01067-16
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摘要: ABSTRACT The Shigella species cause millions of cases watery or bloody diarrhea each year, mostly in children developing countries. While many aspects colonic cell invasion are known, crucial gaps knowledge regarding how the bacteria survive, transit, and regulate gene expression prior to infection remain. In this study, we define mechanisms resistance bile salts build on previous research highlighting induced virulence flexneri strain 2457T following exposure salts. Typical growth patterns were observed within physiological range salts; however, was inhibited at higher concentrations. Interestingly, extended periods led biofilm formation, a conserved phenotype that among members Enterobacteriaceae. Characterization S. biofilms determined both glucose required for dispersion dependent upon depletion, recovered displayed adherence HT-29 cells. RNA-sequencing analysis verified an important salt transcriptional profile 2457T, including drug expression. Finally, functional mutagenesis identified importance AcrAB efflux pump lipopolysaccharide O-antigen synthesis resistance. Our data demonstrate employs multiple survive salts, which may have implications multidrug Furthermore, our work confirms signals activate virulence. This provides insights into likely regulates survival during host transit subsequent infection.