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Infection and Immunity, November 2005, p. 7535-7540, Vol. 73, No. 11
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.11.7535-7540.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

MyD88-Dependent Signaling Contributes to Protection following Bacillus anthracis Spore Challenge of Mice: Implications for Toll-Like Receptor Signaling

Molly A. Hughes,1* Candace S. Green,1 Lisa Lowchyj,1 Gloria M. Lee,2 Vanessa K. Grippe,2 Michael F. Smith Jr.,3 Li-Yun Huang,4 Eric T. Harvill,5 and Tod J. Merkel2

Division of Infectious Diseases,1 Division of Gastroenterology, Department of Internal Medicine, University of Virginia Health Sciences System, Charlottesville, Virginia,3 Laboratory of Respiratory and Special Pathogens, Division of Bacterial, Parasitic and Allergenic Products,2 Laboratory of Plasma Derivatives, Division of Hematology, Center for Biologics Evaluation and Research, Food and Drug Administration, Bethesda, Maryland,4 Immunology Research Laboratories, Department of Veterinary Science, The Pennsylvania State University, University Park, Pennsylvania5

Received 10 May 2005/ Returned for modification 11 July 2005/ Accepted 18 July 2005

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.

* Corresponding author. Mailing address: Department of Internal Medicine, Division of Infectious Diseases, University of Virginia Health Sciences System, P.O. Box 800513, Charlottesville, VA 22908. Phone: (434) 924-5216. Fax: (434) 982-3830. E-mail: mah3x{at}virginia.edu.

Editor: J. T. Barbieri

Infection and Immunity, November 2005, p. 7535-7540, Vol. 73, No. 11
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.11.7535-7540.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



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