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


Por: Ares, Miguel A., Fernandez-Vazquez, Jose L., Rosales-Reyes, Roberto, Dolores Jarillo-Quijada, Ma., von Bargen, Kristine, Torres, Javier, Gonzalez-y-Merchand, Jorge A., Alcantar-Curiel, Maria D., De la Cruz, Miguel A.

Publicada: 9 feb 2016
Resumen:
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 Delta hns mutant and evaluated the role of the H-NS nucleoid protein on the virulence features of K. pneumoniae. A Delta hns 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 Delta hns 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.

Filiaciones:
Hosp Pediat Mexico City, Inst Mexican Seguro Social, Ctr Med Nacl Siglo 21, Unidad Invest Med Enfermedades Infecciosas & Para, Mexico City, DF, Mexico
Inst Politecn Nacl, Dept Microbiol, Escuela Nacl Ciencias Biol, Mexico City, DF, Mexico
Univ Nacl Autonoma Mexico, Fac Med, Unidad Invest Med Expt, Mexico City 04510, DF, Mexico
Univ Bonn, Cell Biol Inst, Bonn, Germany
ISSN: 22352988
Editorial
FRONTIERS RESEARCH FOUNDATION, PO BOX 110, LAUSANNE, 1015, SWITZERLAND, Suiza
Tipo de documento: Article
Volumen: 6 Número: FEB
Páginas:
WOS Id: 000369598500002
ID de PubMed: 26904512

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