| Literature DB >> 18400546 |
Shao-Hung Wang1, Chen Zhang, Mark E Lasbury, Chung-Ping Liao, Pamela J Durant, Dennis Tschang, Chao-Hung Lee.
Abstract
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 PcP indeed exhibited milder pulmonary inflammation. TLR2-/- mouse lungs contained less TNF-alpha and displayed lower levels of NF-kappaB activation during PcP. 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.Entities:
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Year: 2007 PMID： 18400546 PMCID： PMC2423425 DOI： 10.1016/j.micinf.2007.12.014
Source DB: PubMed Journal: Microbes Infect ISSN： 1286-4579 Impact factor: 2.700