| Popis: |
>In recent years, two assumptions have led to a sustained interest in the role played by plasma fibronectin (Fn) in health and disease. The first is that plasma Fn serves as a critical regulator of reticuloendothelial system (RES) function; the second, that subnormal Fn levels are of clinical significance. The structure and known activities of Fn provide the basis for these concepts (reviewed in, 4, 11). Plasma fibronectin has been shown to bind to products of intravascular coagulation, cell debris, denatured and native collagens, and to some bacteria. Its interactions with macrophages, monocytes, and neutrophils facilitate the clearance of Fn-bound targets by the cells of the RES. The clearance promoting capabilities of Fn are, however, limited to the “target particles” to which Fn can bind, and by physiologic factors that are as yet incompletely understood (11). Animal studies have demonstrated a parallelism between Fn levels, RES function, and ultimate mortality following blunt tissue trauma; however, such associations are not found in states of thrombin induced DIC, experimental endotoxemia, gram-negative bacteremia and burns (reviewed in 11). Fn levels in these experimental settings do not necessarily reflect RES function nor perturbations in the complement, coagulation, fibrinolytic, or kinin generating systems. |
