Pulmonary surfactant-associated protein alterations in subjects colonised by Pneumocystis jirovecii with idiopathic interstitial pneumonia
Abstract number: 1733_466
Friaza V., de la Horra C., Respaldiza N., Montes-Cano M.A., Munoz-Lobato F., Morilla R., Rivero L., Martin-Juan J., Varela J.M., Rodriguez-Becerra E., Medrano F.J., Calderon E.J.
Background: Idiopathic Interstitial Pneumonia (IIP) is a heterogeneous group of poorly understood diseases with uncertain etiology. All of them feature an initial inflammatory response that can lead to pulmonary fibrosis in some cases. This initial inflammatory response could be somehow trigger by an infectious agent. It is well known that pulmonary surfactant-associated proteins SP-A and SP-D play an important role in lung host defence. In the same manner, there are evidences that SP-A and SP-D regulate NF-kB and, by this pathway, are able to enhance or suppress inflammatory mediators production. It had been previously reported in vitro and in animal models, that Pneumocystis binds to surfactant proteins and could alter their expression and distribution.
Objectives: To identify possible alterations in Pulmonary Surfactant-associated Protein components in IIP Pneumocystis colonised patients.
Patients and Methods: Bronchoalveolar lavage fluid (BALF) from 40 IIP patients was collected and the identification of P. jirovecii was performed by mt LSU RNAr gene Nested-PCR. SP-A levels were determined by western-blotting following densitometry analysis using 1D Manager Software. SP-D was assayed by commercial available ELISA Kits (Human SP-D ELISA BioVendor). All data obtained were normalised with total protein concentration (quickstart Bradford dye reagent, Biorad) of each sample.
Results:P. jirovecii was identified in 14 out of 40 (35%) IIP patients. The results obtained for surfactant-associated proteins are showed in the following table:
1. A high P. jirovecii colonisation rate in IIP patients has been found.
2. There is a statistical significant SP-D decrease in colonised IIP patients.
3. P. jirovecii could play a role in the physiopathology of this disease through interaction with pulmonary surfactant-associated proteins.
|Session name:||European Society of Clinical Microbiology and Infectious Diseases|
|Location:||ICC, Munich, Germany|
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