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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, 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.

Present address: National Institutes of Health, Bethesda, Md.

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