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Plasminogen Activator Production in a Rat Model of Pneumocystis carinii Pneumonia
Author(s) -
Angelici Elena,
Contini Carlo,
Spezzano Massimiliano,
Romani Roberto,
Carfagna Paolo,
Serra Pietro,
Canipari Rita
Publication year - 2001
Publication title -
microbiology and immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.664
H-Index - 70
eISSN - 1348-0421
pISSN - 0385-5600
DOI - 10.1111/j.1348-0421.2001.tb01291.x
Subject(s) - pneumocystis carinii , biology , pneumonia , microbiology and biotechnology , plasminogen activator , immunology , activator (genetics) , virology , medicine , human immunodeficiency virus (hiv) , endocrinology , pneumocystis jirovecii , biochemistry , gene
Several studies have indicated that the serine protease urokinase‐plasminogen‐activator (uPA) is an important factor in host defense against pulmonary pathogens. To gain a better insight into the role of uPA in Pneumocystis carinii ( P. carinii ) pneumonia (PCP), we evaluated PA production in alveolar macrophages (AMs) obtained from rats with steroid‐induced PCP. Treatment with cortisone acetate favored PCP in 91% of rats. In the bronchoalveolar lavage (BAL) samples of immunosuppressed rats both with and without PCP, we observed a decrease in uPA activity as well as a decrease in cell number. Urokinase‐PA production by AMs was reduced in rats treated with cortisone alone. However, an increase in cell‐associated uPA was observed in rats with PCP. This increase appears to be produced in response to P. carinii infection. In fact, when AMs obtained from untreated healthy or immunosuppressed uninfected rats were challenged with P. carinii , a significant increase in PA activity in cell lysates was observed, though a lower response was obtained in cortisone‐treated animals. Our results suggest that healthy AMs respond to the presence of P. carinii with an increase in uPA production and that this response in immunodepressed rat‐AMs is partially impaired.