Fibrin in peritonitis. V. Fibrin inhibits phagocytic killing of Escherichia coli by human polymorphonuclear leukocytes.

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RESUMO

Fibrin deposition initiated by peritonitis is thought to be an important local defense mechanism because it sequesters and walls off bacterial spillage. However, fibrin has been shown to predispose to residual abscess formation in rat peritonitis model. To examine the potential mechanisms of this effect, fibrin was tested in vitro for its inhibitory effect on neutrophil function. At all concentrations tested (50-1000 mg/dl), fibrin significantly impaired the ability of neutrophils to kill Escherichia coli. This inhibition occurred in a dose dependent fashion with almost complete prevention of killing at the highest concentration tested. Further studies showed that pre-exposure to fibrin did not reduce the neutrophil's ability to degranulate, undergo a respiratory burst, or kill E. coli, indicating that fibrin did not cause irreversible damage to the normal microbicidal functions of the neutrophil. However, fibrin, at physiologic concentrations, significantly impaired phagocytosis of radiolabeled E. coli. The data support the concept that phagocytosis of bacteria is impaired by neutrophils enmeshed in fibrin. Thus, contaminated fibrin could act as a nidus for residual abscesses formation following peritonitis even if an adequate number of normal leukocytes were present.

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