Inflammatory Response in SARS
Date Issued
2004
Date
2004
Author(s)
伍安怡
DOI
922751B002009Y
Abstract
Severe 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.
Publisher
臺北市：國立臺灣大學醫學院免疫學研究所
Type
journal article
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