ABSTRACT
The cells of the inflammatory lesion may supply one or more procoagulants that are able to activate clotting further down the cascade. This chapter examines the critical role of macrophage-mediated fibrin deposition in the pathogenesis of infection. The ability of fibrinolytic agents or anticoagulants to abrogate or prevent various other bacterial infections provides indirect evidence that fibrin deposition is contributory to their pathogenesis. Both in vitro and in vivo studies suggest that the process of bacterial sequestration simultaneously acts to impede bacterial clearance and predisposes to abscess formation. The pathological findings observed within the liver during viral hepatitis include evidence of both intrasinusoidal and parenchymal fibrin deposition. The delayed-type hypersensitivity response is not an infection, but rather an inflammatory response to an antigen challenge. This response is characterized by the appearance of erythema followed by the development of induration. The chapter addresses the critical role of fibrin deposition in the pathogenesis of a variety of infectious and inflammatory disease processes.
