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-α and displayed lower levels of NF-κB 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.
Original language | English |
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Pages (from-to) | 334-341 |
Number of pages | 8 |
Journal | Microbes and Infection |
Volume | 10 |
Issue number | 4 |
DOIs | |
Publication status | Published - Apr 2008 |
Keywords
- Inflammation
- Pneumocystis
- Toll-like receptor 2
ASJC Scopus subject areas
- Microbiology
- Immunology
- Infectious Diseases