RESUMEN
Objective: To investigate the relationship of murine fibrinogen-like protein 2(mfgl2) / fibroleukin with pulmonary impairment in the murine model of severe acute respiratory syndrome(SARS).Methods: The Balb/cJ mice infected with murine hepatitis virus strain 3(MHV-3) through the trachea were observed for the pathological features and virus distribution in different organs.The expressions of both mfgl2 and fibrino in the lungs were determined by in situ hybridization and immunohistochemistry.Results: The MHV-3 infected mice developed typical interstitial pneumonia with extensive hyaline membrane formation in the alveoli,presented micro-vascular thrombosis in the pulmonary vessels and died within 5 days.MHV-3 virus replication was identified in all the organs observed.The specific expression of mfgl2 prothrombinase was noted in the terminal and respiratory bronchioles,alveolar epithelia and infiltrating cells.Conclusion: The characteristics of the pulmonary impairment of SARS in human can be properly simulated by the MHV-3 induced murine model of SARS.The up-regulation of the specific gene mfgl2 in the lungs involved in fibrino deposition and microvascular thrombosis may be largely responsible for SARS-associated pulmonary damages.