title: Contact systems in infectious disease.
abstract: The current state of knowledge of contact coagulation pathways activated by exposure of blood to foreign surfaces such as occur with endothelial damage is reviewed. Changes in the contact proteins in normally occurring and experimentally induced infections in humans are summarized. The use of mutant alpha 1-antitrypsin to inhibit activation of this pathway in experimental porcine sepsis is also described. The principles developed may be applicable in studies of the pathogenesis and treatment of viral hemorrhagic fevers.
authors.affiliation: Thrombosis Research Center, Temple University School of Medicine, Philadelphia, Pennsylvania 19140.
authors.forename: R W
authors.initials: RW
authors.lastname: Colman
mesh_terms: D000818:Animals; D001777:Blood Coagulation; D001778:Blood Coagulation Disorders / Q000209:etiology*; D005172:Factor XI / Q000502:physiology; D005174:Factor XII / Q000502:physiology; D006801:Humans; D007239:Infections / Q000097:blood*; D007704:Kininogens / Q000502:physiology; D011288:Prekallikrein / Q000502:physiology; D011552:Pseudomonas Infections / Q000628:therapy; D011994:Recombinant Proteins / Q000627:therapeutic use; D000515:alpha 1-Antitrypsin / Q000627:therapeutic use
chemical_list: D007704:Kininogens; D011994:Recombinant Proteins; D000515:alpha 1-Antitrypsin; D005174:Factor XII; D005172:Factor XI; D011288:Prekallikrein