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Antimicrobial Agents and Chemotherapy, April 2005, p. 1617-1621, Vol. 49, No. 4
0066-4804/05/$08.00+0     doi:10.1128/AAC.49.4.1617-1621.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Secretion of Proinflammatory Cytokines and Chemokines during Amphotericin B Exposure Is Mediated by Coactivation of Toll-Like Receptors 1 and 2

Raymund R. Razonable,1,2* Martin Henault,2 Linda N. Lee,2 Carmen Laethem,2 Paul A. Johnston,2 Harold L. Watson,2,{dagger} and Carlos V. Paya2

Division of Infectious Diseases and Internal Medicine, Mayo Clinic College of Medicine, Rochester, Minnesota,1 Lilly Research Laboratories, Eli Lilly and Company, Indianapolis, Indiana2

Received 23 September 2004/ Returned for modification 18 November 2004/ Accepted 13 December 2004

Amphotericin B (AmB) is a ligand of toll-like receptor 2 (TLR2). Here, we demonstrate the participation of TLR1 in AmB-induced cell activation that led to the secretion of tumor necrosis factor alpha, interleukin 6 (IL-6), and IL-8. Hence, TLR2-TLR1 coactivation serves as the underlying mechanism for the proinflammatory toxicities associated with AmB.

* Corresponding author. Mailing address: Division of Infectious Diseases, Mayo Clinic and Foundation, 200 First St. SW, Rochester, MN 55905. Phone: (507) 255-6482. E-mail: razonable.raymund{at}mayo.edu.

{dagger} Present address: National Institutes of Health, Bethesda, Md.

Antimicrobial Agents and Chemotherapy, April 2005, p. 1617-1621, Vol. 49, No. 4
0066-4804/05/$08.00+0     doi:10.1128/AAC.49.4.1617-1621.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



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