title: Characterization of cytokine/chemokine profiles of severe acute respiratory syndrome.
abstract: BACKGROUND
  There is currently no optimal treatment or effective drug for severe acute respiratory syndrome (SARS), because the immunopathologic mechanism is poorly understood.
  
  
  OBJECTIVE
  To explore the immune mechanism underlying the pathogenesis of SARS, we studied the expression profile of cytokines/chemokines in the blood and the immunopathology of the lung and lymphoid tissues.
  
  
  METHODS
  Fourteen cytokines/chemokines in the blood of 23 patients with SARS were dynamically screened, using a bead-based multiassay system. Reverse transcription-polymerase chain reaction was performed to amplify mRNA. Histopathology of the lung and lymphoid tissues at autopsy was examined, using methods of immunohistochemistry and double immunofluorescence staining.
  
  
  RESULTS
  Interferon-inducible protein-10 (IP-10) was markedly elevated in the blood during the early stage of SARS, and remained at a high level until convalescence. Moreover, IP-10 was highly expressed in both lung and lymphoid tissues, where monocyte-macrophage infiltration and depletion of lymphocytes were observed. The levels of interleukin-6, interleukin-8, and monocyte chemoattractant protein-1 were concomitantly increased in the blood of the patients with superinfection, and the mRNAs for these cytokines were also increased in lung tissues.
  
  
  CONCLUSIONS
  Induction of IP-10 is a critical event in the initiation of immune-mediated acute lung injury and lymphocyte apoptosis during the development of SARS. Superinfection after the immune injury is the main cause of death. The prompt elevation of interleukin-6, interleukin-8, and monocyte chemoattractant protein-1 is a sign of superinfection, indicating a high risk of death.
authors.affiliation: Department of Pathophysiology, Southern Medical University, Tonghe, Guangzhou 510515, China. yjiang@fimmu.com
authors.forename: Yong
authors.initials: Y
authors.lastname: Jiang
authors.forename: Jun
authors.initials: J
authors.lastname: Xu
authors.forename: Chengzhi
authors.initials: C
authors.lastname: Zhou
authors.forename: Zhenguo
authors.initials: Z
authors.lastname: Wu
authors.forename: Shuqing
authors.initials: S
authors.lastname: Zhong
authors.forename: Jinghua
authors.initials: J
authors.lastname: Liu
authors.forename: Wei
authors.initials: W
authors.lastname: Luo
authors.forename: Tao
authors.initials: T
authors.lastname: Chen
authors.forename: Qinghe
authors.initials: Q
authors.lastname: Qin
authors.forename: Peng
authors.initials: P
authors.lastname: Deng
mesh_terms: D000328:Adult; D017209:Apoptosis / Q000276:immunology; D018932:Chemokine CCL2 / Q000097:blood; D018925:Chemokines / Q000097:blood* / Q000235:genetics; D016207:Cytokines / Q000097:blood* / Q000235:genetics; D005260:Female; D015870:Gene Expression / Q000502:physiology; D006801:Humans; D008168:Lung / Q000276:immunology / Q000473:pathology; D008214:Lymphocytes / Q000276:immunology / Q000473:pathology; D008221:Lymphoid Tissue / Q000473:pathology; D008297:Male; D008856:Microscopy, Fluorescence; D008875:Middle Aged; D012016:Reference Values; D020133:Reverse Transcriptase Polymerase Chain Reaction; D045473:Severe acute respiratory syndrome-related coronavirus / Q000276:immunology; D045169:Severe Acute Respiratory Syndrome / Q000175:diagnosis / Q000276:immunology* / Q000473:pathology; D015163:Superinfection / Q000276:immunology / Q000473:pathology
chemical_list: D018932:Chemokine CCL2; D018925:Chemokines; D016207:Cytokines