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

Microbes and Infection
Shao-Hung WangChao-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.

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Citations

Jun 19, 2010·American Journal of Respiratory Cell and Molecular Biology·Mark E LasburyChao-Hung Lee
Dec 22, 2009·Future Microbiology·Michelle N Kelly, Judd E Shellito
Apr 1, 2014·Microbes and Infection·Chiara RipamontiJoseph A Kovacs
Oct 31, 2008·Journal of the Formosan Medical Association = Taiwan Yi Zhi·Jang-Jih Lu, Chao-Hung Lee
Sep 30, 2010·Immunology Letters·Naja J JannRegine Landmann
Jul 9, 2010·Alcoholism, Clinical and Experimental Research·Melanie D BirdElizabeth J Kovacs
Jun 1, 2011·International Immunopharmacology·Melissa A Kovach, Theodore J Standiford
Dec 3, 2013·The Journal of Immunology : Official Journal of the American Association of Immunologists·Sheila N Bello-IrizarryTerry W Wright
Dec 8, 2010·The Journal of Immunology : Official Journal of the American Association of Immunologists·Makoto InoueMari L Shinohara

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