title: Inflammation inhibitors were remarkably up-regulated in plasma of severe acute respiratory syndrome patients at progressive phase.
abstract: Severe acute respiratory syndrome (SARS) is a severe infectious disease that has affected many countries and regions since 2002. A novel member of the coronavirus, SARS-CoV, has been identified as the causative agent. However, the pathogenesis of SARS is still elusive. In this study, we used 2-D DIGE and MS to analyze the protein profiles of plasma from SARS patients, in the search for proteomic alterations associated with the disease progression, which could provide some clues to the pathogenesis. To enrich the low-abundance proteins in human plasma, two highly abundant proteins, albumin and IgG, were first removed. By comparing the plasma proteins of SARS patients with those of a normal control group, several proteins with a significant alteration were found. The up-regulated proteins were identified as alpha-1 acid glycoprotein, haptoglobin, alpha-1 anti-chymotrypsin and fetuin. The down-regulated proteins were apolipoprotein A-I, transferrin and transthyretin. Most of the proteins showed significant changes (up- or down-regulated) in the progressive phase of disease, and there was a trend back to normal level during the convalescent phase. Among these proteins, the alterations of fetuin and anti-chymotrypsin were further confirmed by Western blotting. Since all the up-regulated proteins identified above are well-known inflammation inhibitors, these results strongly suggest that the body starts inflammation inhibition to sustain the inflammatory response balance in the progression of SARS.
authors.affiliation: Department of Genomics and Proteomics, Beijing Institute of Radiation Medicine, Beijing, PR China.
authors.forename: Jia
authors.initials: J
authors.lastname: Wan
authors.forename: Wei
authors.initials: W
authors.lastname: Sun
authors.forename: Xiaohai
authors.initials: X
authors.lastname: Li
authors.forename: Wantao
authors.initials: W
authors.lastname: Ying
authors.forename: Jingquan
authors.initials: J
authors.lastname: Dai
authors.forename: Xuezhang
authors.initials: X
authors.lastname: Kuai
authors.forename: Handong
authors.initials: H
authors.lastname: Wei
authors.forename: Xue
authors.initials: X
authors.lastname: Gao
authors.forename: Yunping
authors.initials: Y
authors.lastname: Zhu
authors.forename: Ying
authors.initials: Y
authors.lastname: Jiang
authors.forename: Xiaohong
authors.initials: X
authors.lastname: Qian
authors.forename: Fuchu
authors.initials: F
authors.lastname: He
mesh_terms: D000328:Adult; D015153:Blotting, Western; D018450:Disease Progression; D015180:Electrophoresis, Gel, Two-Dimensional; D005260:Female; D006242:Haptoglobins / Q000032:analysis*; D006801:Humans; D008297:Male; D009961:Orosomucoid / Q000032:analysis*; D011228:Prealbumin / Q000032:analysis; D045169:Severe Acute Respiratory Syndrome / Q000097:blood*; D015854:Up-Regulation; D000514:alpha 1-Antichymotrypsin / Q000097:blood*; D000509:alpha-Fetoproteins / Q000032:analysis*
chemical_list: D006242:Haptoglobins; D009961:Orosomucoid; D011228:Prealbumin; D000514:alpha 1-Antichymotrypsin; D000509:alpha-Fetoproteins