期刊
INFECTION AND IMMUNITY
卷 73, 期 11, 页码 7535-7540出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/IAI.73.11.7535-7540.2005
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资金
- NIAID NIH HHS [R21 AI056113, K08 AI050804, R21 AI072469, U54 AI057168, R01 AI034358] Funding Source: Medline
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-alpha) production in C3H/HeN, C3H/HeJ, and C57BL/6J bone marrow-derived macrophages. The ability of heat-killed B. anthracis to induce a TNF-alpha 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.
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