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Titolo:
ADENOVIRUS-MEDIATED EXPRESSION OF CYTOKINE-INDUCED NEUTROPHIL CHEMOATTRACTANT IN RAT-LIVER INDUCES A NEUTROPHILIC HEPATITIS
Autore:
MAHER JJ; SCOTT MK; SAITO JM; BURTON MC;
Indirizzi:
SAN FRANCISCO GEN HOSP,LIVER CTR LAB,1001 POTRERO AVE,BLDG 40,ROOM 4102 SAN FRANCISCO CA 94110 UNIV CALIF SAN FRANCISCO,LIVER CORE CTR SAN FRANCISCO CA 94143 UNIV CALIF SAN FRANCISCO,DEPT MED SAN FRANCISCO CA 94143
Titolo Testata:
Hepatology
fascicolo: 3, volume: 25, anno: 1997,
pagine: 624 - 630
SICI:
0270-9139(1997)25:3<624:AEOCNC>2.0.ZU;2-6
Fonte:
ISI
Lingua:
ENG
Soggetto:
ISCHEMIA-REPERFUSION INJURY; ALCOHOLIC HEPATITIS; CHEMOTACTIC FACTORS; GENE-EXPRESSION; INTERLEUKIN-8; SEQUESTRATION; HEPATOCYTES; ENDOTOXIN; MECHANISM; INVIVO;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
34
Recensione:
Indirizzi per estratti:
Citazione:
J.J. Maher et al., "ADENOVIRUS-MEDIATED EXPRESSION OF CYTOKINE-INDUCED NEUTROPHIL CHEMOATTRACTANT IN RAT-LIVER INDUCES A NEUTROPHILIC HEPATITIS", Hepatology, 25(3), 1997, pp. 624-630

Abstract

C-X-C chemokines are potent chemoattractants that are believed to mediate neutrophilic inflammation in several organs. Recent studies suggest a role for C-X-C chemokines in the pathogenesis of neutrophilic hepatitis but do not prove causation. We investigated the biological consequences of hepatic chemokine production in vivo by transiently overexpressing cytokine-induced neutrophil chemoattractant (CINC), a member of the C-X-C chemokine family, in intact rats. Rats were injected intraportally with a replication-defective recombinant adenovirus containing the CINC complementary DNA (cDNA). Within 4 days, treated animals had high levels of CINC in both liver tissue and plasma. Rats overexpressing CINC exhibited an eightfold increase in circulating neutrophils;they also developed severe hepatic injury, characterized by a 6- to 25-fold increase in plasma transaminases and marked hepatic inflammation on biopsy. Liver disease in CINC-producing rats correlated positively with the number of neutrophils sequestered in the hepatic parenchyma. Tissue injury was attributed directly to chemokine overproduction, because control rats infected with adenoviruses lacking the CINC cDNA did not produce CINC and developed only minor hepatic abnormalities. These experiments provide direct evidence that C-X-C chemokines, when expressed in sufficient quantity in the liver in vivo, induce neutrophilrecruitment and tissue invasion and provoke severe liver injury. The data suggest that C-X-C chemokines have important pathogenic potentialin both clinical and experimental liver disease.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 23/01/21 alle ore 10:17:14