Association between IFN-γexpression and pathological damage of lung tissue during pulmonary tuberculosis
10.3969/j.issn.1006-5725.2014.10.005
- VernacularTitle:肺结核肺组织干扰素-γ表达与其病理损伤间的关系研究
- Author:
Yihao DENG
;
Hongyun HE
;
Maodan TANG
- Publication Type:Journal Article
- Keywords:
Pulmonary tuberculosis;
Interferon-γ;
Tumor necrosis factor-α;
Interleukin-2;
Tissue damage of lung tissue
- From:
The Journal of Practical Medicine
2014;(10):1531-1533
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the relationship between the expression of IFN-γ, IL-2 and TNF-αand pathological damage of lung tissue, and to provide reference values for protection and treatment of pulmonary tuberculosis. Methods BALB/c mice models of pulmonary tuberculosis were established by infection with Mycobacterium tuberculosis H37Rv through the caudal vein. At 0 (not infected),2,4,6W and 8W after infection, the bacterial loads in the lung were performed and the pathological damage of the lung was evaluated, respectively. At the same time, the expression of IFN-γ,IL-2 and TNF-α-positive cells in the lung tissues was detected by immunohistochemistry. Results Two weeks after infection, the expression of IFN-γ, IL-2 and TNF-αpositive cells was obviously increased compared with those at 0 week. The proportion of IFN-γ-positive cells were obviously decreased at 6 weeks (9.25%) to 8 weeks (5.67%) after infection with Mycobacterium tuberculosis H37Rv. At the same stage, there is a limited decrease tendency of TNF-α and IL-2 expression compared with those at 4 weeks after infection, and there was no significant difference compared with those at 2W or 4W after infection. At 8 weeks after infection, the bacterial loads (8.43) in the lung and the scores(17) of pathological damage were significantly increased compared with those at 6 weeks after infection. Conclusion The high expression of IFN-γ, IL-2 and TNF-αprotect lung tissues against MTB infection at the early stage. The decrease of IFN-γexpression is responsible for serious damage of the lung tissues in the persistent infection.
