Secretion of proinflammatory cytokines and chemokines during amphotericin B exposure is mediated by coactivation of toll-like receptors 1 and 2.
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.
Razonable
Raymund R
RR
Division of Infectious Diseases and Internal Medicine, Mayo Clinic College of Medicine, Rochester, Minnesota 55905, USA. razonable.raymund@mayo.edu
Henault
Martin
M
Lee
Linda N
LN
Laethem
Carmen
C
Johnston
Paul A
PA
Watson
Harold L
HL
Paya
Carlos V
CV
D000666:Amphotericin B / Q000276:immunology / Q000494:pharmacology*; D000900:Anti-Bacterial Agents / Q000276:immunology / Q000494:pharmacology*; D002460:Cell Line; D018925:Chemokines / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism*; D006801:Humans; D008562:Membrane Glycoproteins / Q000378:metabolism*; D009000:Monocytes / Q000276:immunology; D011956:Receptors, Cell Surface / Q000378:metabolism*; D051194:Toll-Like Receptor 1; D051195:Toll-Like Receptor 2; D051193:Toll-Like Receptors
D000900:Anti-Bacterial Agents; D018925:Chemokines; D016207:Cytokines; D008562:Membrane Glycoproteins; D011956:Receptors, Cell Surface; C495342:TLR2 protein, human; D051194:Toll-Like Receptor 1; D051195:Toll-Like Receptor 2; D051193:Toll-Like Receptors; D000666:Amphotericin B