Study of cellular apoptosis and its mechanism in lung and other organs of patients with severe acute respiratory syndrome
- VernacularTitle:严重急性呼吸综合征肺脏及肺外器官细胞凋亡及其机制的研究
- Author:
Yanling SUN
;
Jingmin ZHAO
;
Songshan WANG
- Publication Type:Journal Article
- Keywords:
severe acute respiratory syndrome;
apoptosis;
lung;
immune system
- From:
Medical Journal of Chinese People's Liberation Army
1983;0(02):-
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the significance of cellular apoptosis induced by severe acute respiratory syndrome cronovirus (SARS-CoV) in the pathogenesis of SARS. Methods TdT-mediated biotinylated-dUTP nick end ladelling method (TUNEL), and the double immunochemical staining with cytokeratin and CD3, CD8, CD20 and CD68 monoclonal antibodies were used to study the cellular apoptosis in tissue specimens from six patients who died from SARS. Meanwhile, the expression of Fas, Fas ligand (FasL), P53 and Bcl-2 proteins was detected by immunohistochemical method. Results The number of cellular apoptosis was obviously increased in multiple organs from the six patients died from SARS. The cellular apoptosis occurred predominantly in cytokeratin-positive pneumoncytes, terminal bronchiolar epithelium, CD3 + and CD8 + lymphocytes, as well as a part of CD20 + lymphocytes and CD68 + macrophages. Fas protein was mainly expressed in the infiltrated mononuclear cells, while FasL was chiefly expressed in SARS-CoV target cells, especially in the apoptotic cells. In the lung and immune organs, down-regulation of P53 and Bcl-2 expression was found. Conclusion The occurrence of increased and rapid cell apoptosis induced by SARS-CoV might be the main cause of the injuries to the lung and immune system. That the activated lymphocytes which expressed Fas and FasL attack SARS-CoV target cells might be the underlying mechanism of cell apoptosis in SARS. Down-expression of Bcl-2 and P53 proteins might also participate in cell apoptosis induced by SARS-CoV.
