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Pseudomonas aeruginosa Induced Lung Injury Model
Published on: October 29, 2014
Connective tissue responses in acute community-acquired pneumonia
C Nordenbaek1, B Teisner, P Junker
1Department of Internal Medicine C, Section of Rheumatology, Odense University Hospital, 29 Sdr. Boulevard, DK-5000 Odense C, Denmark. claudia@dadlnet.dk
Abstract:
Circulating connective tissue components including the aminoterminal propeptides of type III collagen (PIIINP), type I collagen (PINP) and hyaluronan were determined in patients hospitalised for pneumonia of suspected bacterial origin. Ninety patients were included, 64 of these were followed prospectively for up to 21 days after initiation of therapy. Serum PIIINP was determined by RIA, s-PINP by ELISA, and s-hyaluronan by a radiometric assay. S-PIIINP rose significantly above the zero value within 24 h in both pneumococcal pneumonia (T0: 5.3 microg/l, 95% CI: 2.7-8.1 microg/l vs. T1: 6.7 microg/l, 95% CI: 3.8-9.1, P<0.01) and in pneumonia of unknown aetiology (T0: 4.0 microg/l, 95% CI: 3.6-4.8 vs. T1: 4.5 microg/l, 95% CI: 3.8-5.1, P<0.05) followed by a gradual decline. At T1, S-PIIINP was higher in pneumococcal pneumonia compared with pneumonia of unknown aetiology (P<0.05). By contrast, s-PINP tended to decline within 24 h in both pneumococcal pneumonia (T1: 30 microg/l, 95% CI: 23-40, ns) and in pneumonia of unknown aetiology (T1: 32 microg/l, 95% CI: 22-42, ns) followed by a steady increase. The PINP antigen size distribution remained constant throughout the follow-up period. S-hyaluronan in pneumococcal pneumonia paralleled s-PIIINP reaching a peak value on day 1 (121 microg/l, 95% CI: 65-191, P=0.38). There was a positive correlation between s-PIIINP and C-reactive protein (CRP). The study demonstrates, that community-acquired pneumonia elicits a differentiated mesenchymal response, which is turned down in response to successful antibiotic therapy.
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