Contact systems in infectious disease.
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.
Colman
R W
RW
Thrombosis Research Center, Temple University School of Medicine, Philadelphia, Pennsylvania 19140.
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
D007704:Kininogens; D011994:Recombinant Proteins; D000515:alpha 1-Antitrypsin; D005174:Factor XII; D005172:Factor XI; D011288:Prekallikrein