Secretion of proinflammatory cytokines and chemokines during amphotericin B exposure is mediated by coactivation of toll-like receptors 1 and 2

Raymund R. Razonable, Martin Henault, Linda N. Lee, Carmen Laethem, Paul A. Johnston, Harold L. Watson, Carlos V. Paya

Research output: Contribution to journalArticle

53 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)1617-1621
Number of pages5
JournalAntimicrobial Agents and Chemotherapy
Issue number4
StatePublished - Apr 1 2005


ASJC Scopus subject areas

  • Pharmacology
  • Pharmacology (medical)
  • Infectious Diseases

Cite this