伍安怡2018-07-092018-07-092004http://ntur.lib.ntu.edu.tw//handle/246246/29869Severe acute respiratory syndromes (SARS) stimulate cells of the immune system to produce proinflammatory cytokines and chemokines which mediated acute lung inflammation. To investigate the immunopathogenesis of SARS, we infected a number of human cell lines with SARS-CoV. By immunoflourescent staining with sera from SARS patients, we identified A549 and THP-1 cell lines that are susceptible to the virus. SARS-CoV-infected A549 epithelial cell expressed adhesion molecules, P-selectin and VCAM-1. In addition, total RNA was extracted from the cells to assay for the expression of chemokines. Results of Multi-Probe RNase protection assay demonstrated that the THP-1 cell line expressed CXCL5, CXCL10, CCL2, CCL3, CCL4, and CXCL8 after SARS-CoV infection, while A549 the epithelial cell line expressed only CCL2. Comparing DC-SIGN transfected cells to their parental cell line; we demonstrated that expression of DC-SIGN did not change the kinetics of chemokines induced by SARS-CoV. Chemotaxis assay showed that exposure of peripheral leukocytes to mixture of recombinant chemokines CXCL5, CXCL10, CCL2, CCL3, CCL4, and CXCL8, migration of neutrophils and monocytes out-competed lymphocytes. These data may explain why neutrophils and monocytes were dominant cell types in pulmonary inflammatory response in patients with SARS.application/pdf94631 bytesapplication/pdfzh-TW國立臺灣大學醫學院免疫學研究所journal articlehttp://ntur.lib.ntu.edu.tw/bitstream/246246/29869/1/922751B002009Y.pdf