KMID : 1204320150310020078
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Laboratory Animal Research 2015 Volume.31 No. 2 p.78 ~ p.85
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Tumor necrosis factor-alpha deficiency impairs host defense against Streptococcus pneumoniae
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Jeong Dong-Gu
Seo Jin-Hee Heo Seung-Ho Choi Yang-Kyu Jeong Eui-Suk
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Abstract
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Streptococcus pneumoniae is a major human pathogen that is involved in community-acquired pneumonia. Tumor necrosis factor-alpha (TNF-¥á) is a pro-inflammatory cytokine that activates immune responses against infection, invasion, injury, or inflammation. To study the role of TNF-¥á during S. pneumoniae infection, a murine pneumococcal pneumonia model was used. We intranasally infected C57BL/6J wild-type (WT) and TNF-¥á knockout (KO) mice with S. pneumoniae D39 serotype 2. In TNF-¥á KO mice, continuous and distinct loss of body weight, and low survival rates were observed. Bacterial counts in the lungs and blood of TNF-¥á KO mice were significantly higher than those in WT mice. Histopathological lesions in the spleen of TNF-¥á KO mice were more severe than those in WT mice. In TNF-¥á KO mice, severe depletion of white pulp was observed and the number of apoptotic cells was significantly increased. Interferon-gamma (IFN-¥ã), IL-12p70 and IL-10 levels in serum were significantly increased in TNF-¥á KO mice. TNF-¥á is clearly involved in the regulation of S. pneumoniae infections. Early death and low survival rates of TNF-¥á KO mice were likely caused by a combination of impaired bacterial clearance and damage to the spleen. Our findings suggest that TNF-¥á plays a critical role in protecting the host from systemic S. pneumoniae infection.
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KEYWORD
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Tumor necrosis factor-alpha knockout, Streptococcus pneumoniae, pneumonia
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