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

doi:10.1128/AAC.49.4.1617-1621.2005

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

Infectious Diseases

Research output: Contribution to journal › Article › peer-review

54 Scopus citations

Abstract

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)
Pages (from-to)	1617-1621
Number of pages	5
Journal	Antimicrobial Agents and Chemotherapy
Volume	49
Issue number	4
DOIs	https://doi.org/10.1128/AAC.49.4.1617-1621.2005
State	Published - Apr 2005

ASJC Scopus subject areas

Pharmacology
Pharmacology (medical)
Infectious Diseases

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abstract = "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.",

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AU - Razonable, Raymund R.

AU - Henault, Martin

AU - Lee, Linda N.

AU - Laethem, Carmen

AU - Johnston, Paul A.

AU - Watson, Harold L.

AU - Paya, Carlos V.

PY - 2005/4

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AB - 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.

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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

Abstract

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