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

Shao Hung Wang, Chen Zhang, Mark E. Lasbury, Chung Ping Liao, Pamela J. Durant, Dennis Tschang, Chao Hung Lee

Research output: Contribution to journalArticle

17 Scopus citations


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 languageEnglish (US)
Pages (from-to)334-341
Number of pages8
JournalMicrobes and Infection
Issue number4
StatePublished - Apr 1 2008



  • Inflammation
  • Pneumocystis
  • Toll-like receptor 2

ASJC Scopus subject areas

  • Microbiology
  • Immunology
  • Infectious Diseases

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