Toll-like receptor 2 is required for control of pulmonary infection with Francisella tularensis

被引：101

作者：

Malik, Meenakshi ^{[1
]}

Bakshi, Chandra Shekhar ^{[1
]}

Sahay, Bikash ^{[1
]}

Shah, Aaloki ^{[1
]}

Lotz, Steven A. ^{[1
]}

Sellati, Timothy J. ^{[1
]}

机构：

[1] Albany Med Coll, Ctr Immunol & Microbial Dis, Albany, NY 12208 USA

来源：

INFECTION AND IMMUNITY | 2006年 / 74卷 / 06期

关键词：

D O I：

10.1128/IAI.02030-05

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Toll-like receptor 2 (TLR2) deficiency enhances murine susceptibility to infection by Francisella tularensis as indicated by accelerated mortality, higher bacterial burden, and greater histopathology. Analysis of pulmonary cytokine levels revealed that TLR2 deficiency results in significantly lower levels of tumor necrosis factor alpha and interleukin-6 but increased amounts of gamma interferon and monocyte chemoattractant protein 1. This pattern of cytokine production may contribute to the exaggerated pathogenesis seen in TLR2(-/-) mice. Collectively, these findings suggest that TLR2 plays an important role in tempering the host response to pneumonic tularemia.

引用

页码：3657 / 3662

页数：6

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