The pathophysiologic significance of vitronectin in bacterial pneumonia was studied. The following conclusions were obtained. 1) Plasma vitronectin in healthy persons was 252.3 +/- 65.2 micrograms/ml. The level was markedly decreased to 167.0 +/- 42.7 micrograms/ml in patients with bacterial pneumonia. However, it was gradually increased to the normal levels as recovering with pneumonic lesions. It was also found the negative correlation between plasma vitronectin and CRP (r = -0.7) and plasma fibrinogen (r = -0.6) in the course of pneumonia. 2) Vitronectin was localized on elastic fibers of the basement membrane of bronchial epithelium, the alveolar interstitium and the blood vessels in normal lung tissue by immunohistochemical method. On the other hand, vitronectin was significantly localized on inflammatory sites, in particular, fibrin matrix and fibrous sites in pneumonic lesions. These findings were more dominant in severe pneumonia. The results are suggested that reducing in plasma vitronectin appears to be depended on the vitronectin consumption in pneumonic site. 3) In in vitro experiments, activating PMNs, alveolar macrophages and pulmonary fibroblasts were easy to adhered to vitronectin. This adhesiveness to vitronectin was also observed in the strains of S. pneumoniae, S. aureus, and P. aeruginosa, but not in K. pneumoniae and E. coli. These results suggest that vitronectin plays an important role for host defense mechanism by mediating to cell-bacteria interaction and it promotes the recover of injured tissue by induction with pulmonary fibroblasts.