MRP8/MRP14, CD11b and HLA-DR expression of alveolar macrophages in pneumonia

Activation of alveolar macrophages is characterised by specific alterations to the expression pattern of surface markers under certain pathological co nditions. MRP8/MRP14 and CD1 Ib are involved in the regulation of macrophag e migration and adhesion. HLA-DR regulates the antigen presentation by alve olar macrophages. The aim of this study was to investigate the phenotype of alveolar macrophages in pneumonia particularly in relationship to the chan ges in concentrations of TGF-beta 1 and IL-8. Using cytofluorimetry, we ana lysed the surface expression of MRP8/MRP14, CD11b, and HLA-DR on alveolar m acrophages of 42 pneumonia (PN) patients, 14 patients with interstitial lun g diseases (ILD), five patients with chronic obstructive lung disease (COPD ), and 58 patients without lung disease. Phenotypic characteristics were co rrelated to the concentration of TGF-beta 1 and IL-8 in the bronchoalveolar lavage fluid (BALF) of the same patients. The direct influence of TGF-beta 1 and IL-8 on expression of MRP8/MRP14, CD11b and HLA-DR of cultured monoc ytes and MonoMac cells was analysed. Significantly more MRP8/MRP14 and CD11 b positive macrophages and less HLA-DR-positive macrophages were found in P N but not in ILD or COPD. The percentage of CD11b-positive macrophages corr elated with the TGF-beta 1 as well as the IL-8 concentrations. The amount o f HLA-DR-positive macrophages correlated negatively to the concentration of TGF-beta 1 and IL-8. These findings document a significant activation of a lveolar macrophages during pneumonia. TGF-beta 1 led to a modulation of HLA -DR and MRP8/MRP14-antigen expression in vitro. In conclusion, it was shown that in pneumonia but not in ILD or COPD alveolar macrophages were charact erised by an increased MRP8/MRP14 and CD11b expression and a diminished HLA -DR expression. The characterisation of subpopulations within the alveolar macrophages may be a useful tool for the monitoring of disease progression. (C) 2000 Elsevier Science B.V. All rights reserved.