AUTHOR=Ares Miguel A. , Fernández-Vázquez José L. , Rosales-Reyes Roberto , Jarillo-Quijada Ma. Dolores , von Bargen Kristine , Torres Javier , González-y-Merchand Jorge A. , Alcántar-Curiel María D. , De la Cruz Miguel A. 

TITLE=H-NS Nucleoid Protein Controls Virulence Features of Klebsiella pneumoniae by Regulating the Expression of Type 3 Pili and the Capsule Polysaccharide

JOURNAL=Frontiers in Cellular and Infection Microbiology

VOLUME=6

YEAR=2016

URL=https://www.frontiersin.org/journals/cellular-and-infection-microbiology/articles/10.3389/fcimb.2016.00013

DOI=10.3389/fcimb.2016.00013

ISSN=2235-2988

ABSTRACT=<p><italic>Klebsiella pneumoniae</italic> is an opportunistic pathogen causing nosocomial infections. Main virulence determinants of <italic>K. pneumoniae</italic> 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 Δ<italic>hns</italic> mutant and evaluated the role of the H-NS nucleoid protein on the virulence features of <italic>K. pneumoniae</italic>. A Δ<italic>hns</italic> mutant down-regulated the <italic>mrkA</italic> 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 <italic>K. pneumoniae</italic> adherence to epithelial cells such as A549 and HeLa cells. In infection experiments using RAW264.7 and THP-1 differentiated macrophages, the Δ<italic>hns</italic> 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 <italic>K. pneumoniae</italic>.</p>