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Titolo:
BRADYKININ AND NITRIC-OXIDE IN INFECTIOUS-DISEASE AND CANCER
Autore:
MAEDA H; AKAIKE T; WU J; NOGUCHI Y; SAKATA Y;
Indirizzi:
KUMAMOTO UNIV,SCH MED,DEPT MICROBIOL,HONJO 2-2-1 KUMAMOTO 860 JAPAN
Titolo Testata:
Immunopharmacology
fascicolo: 1-3, volume: 33, anno: 1996,
pagine: 222 - 230
SICI:
0162-3109(1996)33:1-3<222:BANIIA>2.0.ZU;2-9
Fonte:
ISI
Lingua:
ENG
Soggetto:
PLASMA ALPHA-1-PROTEINASE INHIBITOR; VASCULAR-PERMEABILITY; MICROBIAL PROTEINASES; HAGEMAN-FACTOR; HUMAN-COLON; PLASMINOGEN ACTIVATORS; SERRATIAL PROTEASE; RELAXING FACTOR; GUINEA-PIGS; TUMOR;
Keywords:
BACTERIAL INFECTION; BRADYKININ; VASCULAR PERMEABILITY; SHOCK; HYPOTENSION; BACTERIAL DISSEMINATION; TUMOR ASCITES; KALLIKREIN CASCADE; HAGEMAN FACTOR;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
34
Recensione:
Indirizzi per estratti:
Citazione:
H. Maeda et al., "BRADYKININ AND NITRIC-OXIDE IN INFECTIOUS-DISEASE AND CANCER", Immunopharmacology, 33(1-3), 1996, pp. 222-230

Abstract

Vascular pathophysiology at the sites of bacterial infection and cancerous tissues share numerous common events similar to inflammatory tissue. Among them enhanced vascular permeability is the universal and hallmark event mediated by bradykinin. All 16 or more bacterial or fungal proteases we have examined activated one or more steps of the kinin generating Hageman-factor-kallikrein cascade. In the meantime, most oftile microbial proteases rapidly inactivated various plasma inhibitors such as alpha(1)-protease inhibitor and alpha(2)-macroglobulin. Ln addition to the extracellular proteases, bacterial cell wall components(negatively charged LPS) of gram-negative bacteria and teichoic acid moieties of gram-positive bacteria activate the Hageman-factor-kallikrein system and exert hypotensive effects via kinin generation. Endotoxin (LPS) also induces nitric oxide synthase (NOS) which appears to exhibit a rather slow, but significant, effect in relaxing the vascular tone of the infected animal (thus hypotension). Furthermore, bacterial proteases can activate the matrix metalloproteinase (collagenase) resulting in exacerbation of tissue injury in the diseased animal. Many tumor sells or tissues excrete plasminogen activator, and hence activateplasminogen. The plasmin thus generated activates procollagenases. aswell as the Hageman-factor-kallikreim system, resulting in pronouncedextravasation. Fluid accumulation in pleural and ascitic carcinomatoses is largely due to the activated bradykinin-generating system. We can also demonstrate and control enhanced vascular permeability using kallikrein inhibitors, especially the polymer-conjugated soybean trypsininhibitor which exhibits a prolonged plasma t(1/2), kinin antagonists, NOS inhibitors, NO scavengers, inhibitors of prostaglandins and others. Bacterial proteases induce shock in mice which can be prevented bythe soybean trypsin inhibitor by blocking the kallikrein-kinin cascade. Therapeutic use of kinin antagonists and a kallikrein inhibitor hasbeen made for infectious diseases such as septicemia and in tumor pathology.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 05/12/20 alle ore 08:14:29