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Titolo:
GRANULOCYTE-MACROPHAGE COLONY-STIMULATING FACTOR - INVOLVEMENT IN CONTROL OF TRYPANOSOMA-CRUZI INFECTION IN MICE
Autore:
FONTT EO; HEIRMAN C; THIELEMANS K; VRAY B;
Indirizzi:
FREE UNIV BRUSSELS,FAC MED,EXPTL IMMUNOL LAB,CP 615,808 ROUTE LENNIK B-1070 BRUSSELS BELGIUM FREE UNIV BRUSSELS,FAC MED,EXPTL IMMUNOL LAB B-1070 BRUSSELS BELGIUM FREE UNIV BRUSSELS,FAC GENEESKUNDE,FYSIOL LAB BRUSSELS BELGIUM
Titolo Testata:
Infection and immunity
fascicolo: 8, volume: 64, anno: 1996,
pagine: 3429 - 3434
SICI:
0019-9567(1996)64:8<3429:GCF-II>2.0.ZU;2-8
Fonte:
ISI
Lingua:
ENG
Soggetto:
TUMOR-NECROSIS-FACTOR; EXPERIMENTAL CHAGAS-DISEASE; GROWTH-FACTOR-BETA; INTERFERON-GAMMA; IMMUNE-RESPONSES; MYCOBACTERIUM-AVIUM; HUMAN MONOCYTES; FACTOR-ALPHA; IFN-GAMMA; MECHANISM;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
42
Recensione:
Indirizzi per estratti:
Citazione:
E.O. Fontt et al., "GRANULOCYTE-MACROPHAGE COLONY-STIMULATING FACTOR - INVOLVEMENT IN CONTROL OF TRYPANOSOMA-CRUZI INFECTION IN MICE", Infection and immunity, 64(8), 1996, pp. 3429-3434

Abstract

Several cytokines play crucial roles in Trypanosoma cruzi infection in mice, but the involvement of endogenous granulocyte-macrophage colony-stimulating factor (GM-CSF) is poorly documented. This report shows that T, cruzi infection of mice triggered an early and sharp increase in plasma GM-CSF during the ascending phase of parasitemia. The plasmaGM-CSF concentration remained stable at the peak of parasitemia and subsequently increased in those mice that survived to the acute phase. GM-CSF level increased again sharply, while parasitemia was rapidly decreasing. Finally, GM-CSF was undetectable, soon after the disappearance of circulating parasites. Injection of T. cruzi-infected mice with neutralizing anti-GM-CSF monoclonal antibodies induced the early appearance of parasitemia and aggravated cumulative mortality. In contrast,recombinant mouse GM-CSF (rmGM-CSF) caused sharp decreases in both parasitemia and cumulative mortality in T, cruzi-infected mice, Peritoneal macrophages from rmGM-CSF-treated and infected or uninfected mice were less infected ex vivo than those from control mice. Taken together, these data demonstrate the protective action of endogenous GM-CSF inT. cruzi infection. Neutralization of endogenous GM-CSF aggravates infection, while exogenous rmGM-CSF decreases both parasitemia and host mortality.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 10/07/20 alle ore 12:03:29