Correction of serum opsonic defects after burn and sepsis by opsonic fibronectin administration.
Opsonic fibronectin modulates reticuloendothelial (RE) uptake of nonbacterial particulates, as well as some bacterial strains, and may thus play an important role in host defense against sepsis after burn injury. We evaluated the relationship between burn injury, sepsis, and opsonic fibronectin levels in rats, as well as the ability to reverse the acute opsonic deficiency after burn injury by administration of purified opsonic fibronectin. Burn injury resulted in an acute (within one hour) depletion of opsonic fibronectin (from 341 +/- 30 to 98 +/- 7 mg/L) that was correctable by administration of purified opsonic fibronectin when accompanied by moderate sepsis, while burn injury plus severe sepsis (level, 168 +/- 30 mg/L) limited attempted restoration of normal opsonic levels (level, 121 +/- 18 mg/L). The in vitro serum opsonic deficit was partially correctable (from 2.2% to 6.7% of the injected dose per 100 mg), while in vivo RE functional deficits could not be corrected. We conclude that the acute postburn deficiency in opsonic fibronectin is amenable to repletion therapy; however, many additional factors may contribute to acute RE failure after burn injury.
D000818:Animals; D002056:Burns / Q000276:immunology*; D005353:Fibronectins / Q000276:immunology*; D012157:Mononuclear Phagocyte System / Q000276:immunology; D009895:Opsonin Proteins / Q000276:immunology*; D011817:Rabbits; D051381:Rats; D011919:Rats, Inbred Strains; D018805:Sepsis / Q000276:immunology*; D013203:Staphylococcal Infections / Q000276:immunology*
D005353:Fibronectins; D009895:Opsonin Proteins