Journal
JOURNAL OF INFECTIOUS DISEASES
Volume 214, Issue 12, Pages 1865-1875Publisher
OXFORD UNIV PRESS INC
DOI: 10.1093/infdis/jiw451
Keywords
CD36; Klebsiella pneumoniae; macrophage; host defense; multi-drug resistant K. pneumoniae; pneumonia; hypermucoviscous strains
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Funding
- Howard Hughes Medical Institute
- National Institutes of Health [R01 HL086884, R21 AI119042, P01 HL114453]
- Flight Attendant Medical Research Institute
- Vascular Medicine Institute
- Hemophilia Center of Western Pennsylvania
- Institute for Transfusion Medicine
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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.
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