Failure of fibronectin as an opsonin in the host defence system: a case of competitive self inhibition?
In the course of various clinical conditions, consumption of opsonic fibronectin is thought to impair the function of the reticuloendothelial (RE) host defence system. Despite evidence to support its central role in host defence, measurements of circulating fibronectin levels appear to have limited diagnostic or prognostic value. It seems that the problem may be more complex than a simple depletion of fibronectin. It is proposed that the structure of fibronectin can allow a condition of opsonic dysfunction to arise in certain patients, irrespective of the concentration of immunoreactive fibronectin. Fibronectin fragments bound to the target particles (fibrin aggregates, tissue debris, microorganisms) would prevent the binding of fibronectin and so inhibit phagocytosis by cells of the RE system.
D001424:Bacterial Infections / Q000097:blood; D002056:Burns / Q000097:blood; D005353:Fibronectins / Q000097:blood / Q000172:deficiency / Q000502:physiology*; D006801:Humans; D008954:Models, Biological; D012157:Mononuclear Phagocyte System / Q000276:immunology*; D009895:Opsonin Proteins / Q000502:physiology*; D010447:Peptide Hydrolases / Q000096:biosynthesis / Q000097:blood; D011480:Protease Inhibitors / Q000097:blood; D013211:Staphylococcus aureus / Q000378:metabolism; D014947:Wounds and Injuries / Q000097:blood
D005353:Fibronectins; D009895:Opsonin Proteins; D011480:Protease Inhibitors; D010447:Peptide Hydrolases