Citation: Wei-ming YAN, Jia-quan HUANG, Xiao-ping LUO, Qin NING. Expression of Prothrombinase/fibroleukin Gene fg12 in Lung Impairment in a Murine Severe Acute Respiratory Syndrome Model .VIROLOGICA SINICA, 2007, 22(3) : 181-192.

Expression of Prothrombinase/fibroleukin Gene fg12 in Lung Impairment in a Murine Severe Acute Respiratory Syndrome Model

  • Corresponding author: Qin NING, qning@tjh.tjmu.edu.cn
  • Received Date: 31 October 2006
    Accepted Date: 25 December 2006
    Available online: 01 June 2007

    Fund Project: National Science Fund for Distinguished Young Investigators 30123019National Science Fund for Distinguished Young Investigators 30225040National 973 project of Chnia for SARS study 2003CB514112Ministry of Education of China for SARS study 2003-18

  • To evaluate the role of murine fibrinogen like protein 2 (mfgl2) /fibroleukin in lung impairment in Severe acute respiratory syndrome (SARS), a murine SARS model induced by Murine hepatitis virus strain 3 (MHV-3) through trachea was established. Impressively, all the animals developed interstitial pneumonia with extensive hyaline membranes formation within alveoli, and presence of micro-vascular thrombosis in the pulmonary vessels. MHV-3 nucleocapsid gene transcripts were identified in multiple organs including lungs, spleen etc. As a representative proinflammatory gene, mfgl2 prothrombinase expression was evident in terminal and respiratory bronchioles, alveolar epithelia and infiltrated cells in the lungs associated with fibrin deposition and micro-vascular thrombosis. In summary, the established murine SARS model could mimic the pathologic characteristics of lungs in patients with SARS. Besides the physical damages due to virus replication in organs, the up-regulation of novel gene mfgl2 in lungs may play a vital role in the development of SARS associated lung damage.

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    Expression of Prothrombinase/fibroleukin Gene fg12 in Lung Impairment in a Murine Severe Acute Respiratory Syndrome Model

      Corresponding author: Qin NING, qning@tjh.tjmu.edu.cn
    • 1. Laboratory of Infectious Immunology
    • 2. Department of Infectious Disease
    • 3. Department of Pediatrics, Tongji Hospital of Tongji Medical College, Huazhong University of Science & Technology, Wuhan 430030, China
    Fund Project:  National Science Fund for Distinguished Young Investigators 30123019National Science Fund for Distinguished Young Investigators 30225040National 973 project of Chnia for SARS study 2003CB514112Ministry of Education of China for SARS study 2003-18

    Abstract: To evaluate the role of murine fibrinogen like protein 2 (mfgl2) /fibroleukin in lung impairment in Severe acute respiratory syndrome (SARS), a murine SARS model induced by Murine hepatitis virus strain 3 (MHV-3) through trachea was established. Impressively, all the animals developed interstitial pneumonia with extensive hyaline membranes formation within alveoli, and presence of micro-vascular thrombosis in the pulmonary vessels. MHV-3 nucleocapsid gene transcripts were identified in multiple organs including lungs, spleen etc. As a representative proinflammatory gene, mfgl2 prothrombinase expression was evident in terminal and respiratory bronchioles, alveolar epithelia and infiltrated cells in the lungs associated with fibrin deposition and micro-vascular thrombosis. In summary, the established murine SARS model could mimic the pathologic characteristics of lungs in patients with SARS. Besides the physical damages due to virus replication in organs, the up-regulation of novel gene mfgl2 in lungs may play a vital role in the development of SARS associated lung damage.