CD36 Provides Host Protection Against Klebsiella pneumoniae Intrapulmonary Infection by Enhancing Lipopolysaccharide Responsiveness and Macrophage Phagocytosis

Klebsiella pneumoniae remains an important cause of intrapulmonary infection and invasive disease worldwide. K. pneumoniae can evade serum killing and phagocytosis primarily through the expression of a polysaccharide capsule, but its pathogenicity is also influenced by host factors. We examined whet...

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Bibliographic Details
Published in:	The Journal of infectious diseases Vol. 214; no. 12; pp. 1865 - 1875
Main Authors:	Olonisakin, Tolani F., Li, Huihua, Xiong, Zeyu, Kochman, Elizabeth J. K., Yu, Minting, Qu, Yanyan, Hulver, Mei, Kolls, Jay K., St. Croix, Claudette, Doi, Yohei, Nguyen, Minh-Hong, Shanks, Robert M. Q., Mallampalli, Rama K., Kagan, Valerian E., Ray, Anuradha, Silverstein, Roy L., Ray, Prabir, Lee, Janet S.
Format:	Journal Article
Language:	English
Published:	United States Oxford University Press 15-12-2016
Subjects:	Animals CD36 Antigens - metabolism Female Host-Pathogen Interactions Klebsiella Infections - immunology Klebsiella pneumoniae - immunology Lipopolysaccharides - immunology Macrophages - immunology Macrophages - microbiology Major and Brief Reports Male Mice, Inbred C57BL Mice, Knockout PATHOGENESIS AND HOST RESPONSE Phagocytosis Pneumonia, Bacterial - immunology multi-drug resistant K. pneumoniae pneumonia host defense hypermucoviscous strains macrophage CD36 Klebsiella pneumoniae
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Summary:	Klebsiella pneumoniae remains an important cause of intrapulmonary infection and invasive disease worldwide. K. pneumoniae can evade serum killing and phagocytosis primarily through the expression of a polysaccharide capsule, but its pathogenicity is also influenced by host factors. We examined whether CD36, a scavenger receptor that recognizes pathogen and modified self ligands, is a host determinant of K. pneumoniae pathogenicity. Despite differences in serum sensitivity and virulence of 3 distinct K. pneumoniae (hypermucoviscous K1, research K2, and carbapenemase-producing ST258) strains, the absence of CD36 significantly increased host susceptibility to acute intrapulmonary infection by K. pneumoniae, regardless of strain. We demonstrate that CD36 enhances LPS responsiveness to K. pneumoniae to increase downstream cytokine production and macrophage phagocytosis that is independent of polysaccharide capsular antigen. Our study provides new insights into host determinants of K. pneumoniae pathogenicity and raises the possibility that functional mutations in CD36 may predispose individuals to K. pneumoniae syndromes.
Bibliography:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Presented in part: Howard Hughes Medical Institute Science Meeting, Chevy Chase, Maryland, November 2015.
ISSN:	0022-1899 1537-6613
DOI:	10.1093/infdis/jiw451