Cutting edge: MyD88 controls phagocyte NADPH oxidase function and killing of gram-negative bacteria

J Immunol. 2005 Nov 1;175(9):5596-600. doi: 10.4049/jimmunol.175.9.5596.

Abstract

MyD88 is an adaptor protein for the TLR family of proteins that has been implicated as a critical mediator of innate immune responses to pathogen detection. In this study, we report that MyD88 plays a crucial role in killing Gram-negative bacteria by primary macrophages via influencing NADPH oxidase function. Peritoneal macrophages from MyD88-/- mice exhibited a marked inability to kill Escherichia coli (F18) or an attenuated strain of Salmonella typhimurium (sseB) in vitro. This defect in killing was due to diminished NADPH oxidase-mediated production of superoxide anion in response to bacteria by MyD88-/- phagocytes as a consequence of defective NADPH oxidase assembly. Defective oxidase assembly in MyD88-deficient macrophages resulted from impaired p38 MAPK activation and subsequent phosphorylation of p47phox. Together these data demonstrate a pivotal role for MyD88 in killing Gram-negative bacteria via modulation of NADPH oxidase activity in phagocytic cells.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Adaptor Proteins, Signal Transducing / physiology*
  • Animals
  • Antigens, Differentiation / physiology*
  • Gram-Negative Bacteria / immunology*
  • Macrophages / enzymology*
  • Macrophages / immunology*
  • Mice
  • Mice, Inbred C57BL
  • Myeloid Differentiation Factor 88
  • NADPH Oxidases / physiology*
  • Phagocytosis*
  • Phosphorylation
  • Receptors, Immunologic / physiology*
  • p38 Mitogen-Activated Protein Kinases / physiology

Substances

  • Adaptor Proteins, Signal Transducing
  • Antigens, Differentiation
  • Myd88 protein, mouse
  • Myeloid Differentiation Factor 88
  • Receptors, Immunologic
  • NADPH Oxidases
  • p38 Mitogen-Activated Protein Kinases