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 language||English (US)|
|Number of pages||5|
|Journal||Antimicrobial Agents and Chemotherapy|
|State||Published - Apr 2005|
ASJC Scopus subject areas
- Pharmacology (medical)
- Infectious Diseases