- Author:
Dong Gu JEONG
1
;
Jin Hee SEO
;
Seung Ho HEO
;
Yang Kyu CHOI
;
Eui Suk JEONG
Author Information
- Publication Type:Original Article
- Keywords: Tumor necrosis factor-alpha knockout; Streptococcus pneumoniae; pneumonia
- MeSH: Animals; Bacterial Load; Body Weight; Humans; Inflammation; Interferon-gamma; Interleukin-10; Lung; Mice; Pneumonia; Pneumonia, Pneumococcal; Spleen; Streptococcus pneumoniae*; Survival Rate; Tumor Necrosis Factor-alpha*
- From:Laboratory Animal Research 2015;31(2):78-85
- CountryRepublic of Korea
- Language:English
- Abstract: Streptococcus pneumoniae is a major human pathogen that is involved in community-acquired pneumonia. Tumor necrosis factor-alpha (TNF-alpha) is a pro-inflammatory cytokine that activates immune responses against infection, invasion, injury, or inflammation. To study the role of TNF-alpha during S. pneumoniae infection, a murine pneumococcal pneumonia model was used. We intranasally infected C57BL/6J wild-type (WT) and TNF-alpha knockout (KO) mice with S. pneumoniae D39 serotype 2. In TNF-alpha KO mice, continuous and distinct loss of body weight, and low survival rates were observed. Bacterial counts in the lungs and blood of TNF-alpha KO mice were significantly higher than those in WT mice. Histopathological lesions in the spleen of TNF-alpha KO mice were more severe than those in WT mice. In TNF-alpha KO mice, severe depletion of white pulp was observed and the number of apoptotic cells was significantly increased. Interferon-gamma (IFN-gamma), IL-12p70 and IL-10 levels in serum were significantly increased in TNF-alpha KO mice. TNF-alpha is clearly involved in the regulation of S. pneumoniae infections. Early death and low survival rates of TNF-alpha KO mice were likely caused by a combination of impaired bacterial clearance and damage to the spleen. Our findings suggest that TNF-alpha plays a critical role in protecting the host from systemic S. pneumoniae infection.