The possible mechanism of the acute lung injury induced by S protein of SARS-CoV
- VernacularTitle:严重急性呼吸综合征冠状病毒S蛋白启动急性肺损伤的可能机制
- Author:
Guohua YAO
;
Xinyan YANG
;
Jun XU
- Publication Type:Journal Article
- Keywords:
Severe acute respiratory syndrome;
Coronavirus;
S protein;
Airway epithelial-cell
- From:
Journal of Medical Postgraduates
2003;0(08):-
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To investigate the role of the recombinant S protein of SARS-CoV in the induction of chemokine IP-10 and other cytokines in airway epithelial cells and immunocytes. Methods: Using insect-baculovirus expression system and Nickel affinity Magnet Beads, S protein of SARS-CoV was produced and then used to stimulate cultured human bronchial epithelial cells (16HBE), human peripheral blood mononuclear cells(PBMC), human peripheral blood monocytes and alveolar macrophages. The levels of IP-10 and the cytokines involved in immunoreaction in response to virus infection were detected in the supernatants of those cells cultured with the S protein by liquid chip system. Results: Under normal condition, no detectable IP-10 was found in 16HBE. A high level of IP-10(79.97? 13.81) pg/ml was detected in the 16HBE 12 hrs after being treated with the S protein, and the induction of IP-10 by S protein displayed at a significant quantity-effect reaction, but not in PBMC, monocytes and alveolar macrophages. In contrast, IFN-? was able to induce the production of IP-10 in either 16HBE or the immunocytes. Conclusion: 1.S protein of SARS-CoV can induce a high level of IP-10 in lung epithelial cells at early stage after the virus infection, which may initiate the process of the immune damage in the lung. 2. S protein of SARS-CoV induces the production of IP-10 by a way of IFN-? independent.
