MyD88-dependent signaling contributes to protection following Bacillus anthracis spore challenge of mice: Implications for toll-like receptor signaling

Molly A. Hughes, Candace S. Green, Lisa Lowchyj, Gloria M. Lee, Vanessa K. Grippe, Michael F. Smith, Li Yun Huang, Eric T. Harvill, Tod J. Merkel

Research output: Contribution to journalArticlepeer-review

42 Scopus citations

Abstract

Bacillus anthracis is a spore-forming, gram-positive organism that is the causative agent of the disease anthrax. Recognition of Bacillus anthracis by the host innate immune system likely plays a key protective role following infection. In the present study, we examined the role of TLR2, TLR4, and MyD88 in the response to B. anthracis. Heat-killed Bacillus anthracis stimulated TLR2, but not TLR4, signaling in HEK293 cells and stimulated tumor necrosis factor alpha (TNF-α) production in C3H/HeN, C3H/HeJ, and C57BL/6J bone marrow-derived macrophages. The ability of heat-killed B. anthracis to induce a TNF-α response was preserved in TLR2-/- but not in MyD88 -/- macrophages. In vivo studies revealed that TLR2-/- mice and TLR4-deficient mice were resistant to challenge with aerosolized Sterne strain spores but MyD88-/- mice were as susceptible as A/J mice. We conclude that, although recognition of B. anthracis occurs via TLR2, additional MyD88-dependent pathways contribute to the host innate immune response to anthrax infection.

Original languageEnglish (US)
Pages (from-to)7535-7540
Number of pages6
JournalInfection and Immunity
Volume73
Issue number11
DOIs
StatePublished - Nov 2005

All Science Journal Classification (ASJC) codes

  • Parasitology
  • Microbiology
  • Immunology
  • Infectious Diseases

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