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

被引：56

作者：

Razonable, RR

Henault, M

Lee, LN

Laethem, C

Johnston, PA

Watson, HL

Paya, CV

机构：

[1] Mayo Clin & Mayo Fdn, Div Infect Dis & Internal Med, Rochester, MN 55905 USA

[2] Eli Lilly & Co, Lilly Res Labs, Indianapolis, IN 46285 USA

来源：

ANTIMICROBIAL AGENTS AND CHEMOTHERAPY | 2005年 / 49卷 / 04期

关键词：

D O I：

10.1128/AAC.49.4.1617-1621.2005

中图分类号：

Q93 [微生物学];

学科分类号：

071005 ; 100705 ;

摘要：

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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页码：1617 / 1621

页数：5

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