CD36 provides host protection against klebsiella pneumoniae intrapulmonary infection by enhancing lipopolysaccharide responsiveness and macrophage phagocytosis

Tolani F. Olonisakin, Huihua Li, Zeyu Xiong, Elizabeth J.K. Kochman, Minting Yu, Yanyan Qu, Mei Hulver, Jay K. Kolls, Claudette St Croix, Yohei Doi, Minh Hong Nguyen, Robert M.Q. Shanks, Rama K. Mallampalli, Valerian E. Kagan, Anuradha Ray, Roy L. Silverstein, Prabir Ray, Janet S. Lee

Research output: Contribution to journalArticlepeer-review

28 Scopus citations

Abstract

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.

Original languageEnglish
Pages (from-to)1865-1875
Number of pages11
JournalJournal of Infectious Diseases
Volume214
Issue number12
DOIs
StatePublished - Dec 1 2016

Keywords

  • CD36
  • Host defense
  • Hypermucoviscous strains
  • Klebsiella pneumoniae
  • Macrophage
  • Multi-drug resistant K. pneumoniae
  • Pneumonia

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