Title |
H-NS Nucleoid Protein Controls Virulence Features of Klebsiella pneumoniae by Regulating the Expression of Type 3 Pili and the Capsule Polysaccharide
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Published in |
Frontiers in Cellular and Infection Microbiology, February 2016
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DOI | 10.3389/fcimb.2016.00013 |
Pubmed ID | |
Authors |
Miguel A. Ares, José L. Fernández-Vázquez, Roberto Rosales-Reyes, Ma. Dolores Jarillo-Quijada, Kristine von Bargen, Javier Torres, Jorge A. González-y-Merchand, María D. Alcántar-Curiel, Miguel A. De la Cruz |
Abstract |
Klebsiella pneumoniae is an opportunistic pathogen causing nosocomial infections. Main virulence determinants of K. pneumoniae are pili, capsular polysaccharide, lipopolysaccharide, and siderophores. The histone-like nucleoid-structuring protein (H-NS) is a pleiotropic regulator found in several gram-negative pathogens. It has functions both as an architectural component of the nucleoid and as a global regulator of gene expression. We generated a Δhns mutant and evaluated the role of the H-NS nucleoid protein on the virulence features of K. pneumoniae. A Δhns mutant down-regulated the mrkA pilin gene and biofilm formation was affected. In contrast, capsule expression was derepressed in the absence of H-NS conferring a hypermucoviscous phenotype. Moreover, H-NS deficiency affected the K. pneumoniae adherence to epithelial cells such as A549 and HeLa cells. In infection experiments using RAW264.7 and THP-1 differentiated macrophages, the Δhns mutant was less phagocytized than the wild-type strain. This phenotype was likely due to the low adherence to these phagocytic cells. Taken together, our data indicate that H-NS nucleoid protein is a crucial regulator of both T3P and CPS of K. pneumoniae. |
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Demographic breakdown
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Researcher | 8 | 8% |
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