Decreased inflammatory response in Toll-like receptor 2 knockout mice is associated with exacerbated Pneumocystis pneumonia

被引：17

作者：

Wang, Shao-Hung ^{[2
]}

Zhang, Chen ^{[1
]}

Lasbury, Mark E. ^{[1
]}

Liao, Chung-Ping ^{[1
]}

Durant, Pamela J. ^{[1
]}

Tschang, Dennis ^{[1
]}

Lee, Chao-Hung ^{[1
]}

机构：

[1] Indiana Univ, Sch Med, Dept Pathol & Lab Med, Indianapolis, IN 46202 USA

[2] I Shou Univ, Dept Med Res, E DA Hosp, Kaohsiung 824, Taiwan

来源：

MICROBES AND INFECTION | 2008年 / 10卷 / 04期

关键词：

Pneumocystis; Toll-like receptor 2; inflammation;

D O I：

10.1016/j.micinf.2007.12.014

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Pneumocystis pneumonia (PcP) is marked by substantial inflammatory damage to the lung. We have found that Toll-like receptor 2 (TLR2) mediates macrophage inflammatory responses to Pneumocystis and hypothesized that TLR2 deficiency would lead to less severe inflammation and milder lung injury during PcP. Histopathology examination showed that TLR2-/- mice with PeP indeed exhibited milder pulmonary inflammation. TLR2-/- mouse lungs contained less TNF-alpha and displayed lower levels of NF-kappa B activation during PcR However, TLR2-/- mice with PcP displayed increased severity in symptoms and organism burden. The increased organism burden is likely due to defects in protective mechanisms in TLR2-/- mice. mRNA levels of the inducible nitric oxide synthase and NADPH oxidase p47phox, as well as nitric oxide levels in the lungs, were decreased in TLR2-/- PcP mice. Taken together, this study shows that TLR2-mediated inflammatory responses contribute to a certain degree to the clearance of Pneumocystis organism in mice. (C) 2007 Elsevier Masson SAS. All rights reserved.

引用

页码：334 / 341

页数：8

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