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Published on: April 14, 2011
Expression and DNA microarray analysis of a platelet activating factor-related molecule in severe pneumonia in mice
Masafumi Seki1, Kosuke Kosai, Atsuko Hara
1Department of Molecular Microbiology and Immunology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki 852-8501, Japan. seki@nagasaki-u.ac.jp
Abstract:
Platelet-activating factor (PAF) is a critical mediator of severe inflammatory diseases such as pneumonia, and the PAF-receptor (PAFR) is known to be an anchor for Streptococcus pneumoniae attachment to lung epithelial cells. We conducted a DNA microarray analysis to detect critical factors that mediate fulminant pneumonia due to influenza virus and S. pneumoniae co-infection in mice. Among the factors detected, levels of PAF-acetyl hydrolase (PAF-AH), which functions as inactivated PAF, were significantly increased, and PAFR was expressed in co-infected mouse lungs, as compared to the respective levels in mice infected with either S. pneumoniae or virus alone. Significantly elevated PAF-AH enzymatic activity was observed in the co-infected mouse lung, suggesting that co-infection activated PAF-related factors. These findings suggest that PAF and related molecules play important roles in fulminant pneumonia due to influenza virus infection, especially when severe bacterial pneumonia is complicated by co-infection with influenza virus.
Insights
Co-infection with influenza virus and Streptococcus pneumoniae significantly increases platelet-activating factor (PAF) and its receptor (PAFR) in mouse lungs, indicating their role in severe pneumonia.
Area of Science:
- Immunology
- Microbiology
- Pulmonary Medicine
Background:
- Platelet-activating factor (PAF) is a key mediator in severe inflammatory conditions like pneumonia.
- The PAF receptor (PAFR) facilitates Streptococcus pneumoniae attachment to lung cells.
- Influenza virus and S. pneumoniae co-infection can lead to severe pneumonia.
Purpose of the Study:
- To identify critical factors involved in fulminant pneumonia caused by influenza virus and S. pneumoniae co-infection.
- To investigate the role of PAF and related molecules in this co-infection model.
Main Methods:
- DNA microarray analysis in a mouse model of co-infection.
- Measurement of PAF-acetyl hydrolase (PAF-AH) levels and enzymatic activity.
- Assessment of PAFR expression in lung tissue.
Main Results:
- Co-infected mouse lungs showed significantly increased PAF-AH levels and PAFR expression compared to single infections.
- Elevated PAF-AH enzymatic activity was observed in co-infected lungs.
- These findings suggest activation of PAF-related pathways during co-infection.
Conclusions:
- PAF and associated molecules are crucial in severe pneumonia resulting from influenza virus and S. pneumoniae co-infection.
- The study highlights the complex inflammatory response during polymicrobial respiratory infections.
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