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Titolo:
TNF-alpha and IL-10 modulate the induction of apoptosis by virulent Mycobacterium tuberculosis in murine macrophages
Autore:
Rojas, M; Olivier, M; Gros, P; Barrera, LF; Garcia, LF;
Indirizzi:
UnivrAntioquia, Fac Med, Ctr Invest Med, Lab Cent Invest,Grp Inmunol Celula Univ Antioquia Medellin Colombia ed, Lab Cent Invest,Grp Inmunol Celula UnivP4,val, Ctr Hosp Univ Quebec, Ctr Rech, Lab Infectiol, St Foy, PQ G1K 7 Univ Laval St Foy PQ Canada G1K 7P4 Rech, Lab Infectiol, St Foy, PQ G1K 7 McGill Univ, Dept Biochem, Montreal, PQ, Canada McGill Univ Montreal PQ Canada Univ, Dept Biochem, Montreal, PQ, Canada
Titolo Testata:
JOURNAL OF IMMUNOLOGY
fascicolo: 10, volume: 162, anno: 1999,
pagine: 6122 - 6131
SICI:
0022-1767(19990515)162:10<6122:TAIMTI>2.0.ZU;2-5
Fonte:
ISI
Lingua:
ENG
Soggetto:
TUMOR-NECROSIS-FACTOR; OXIDE-INDUCED APOPTOSIS; INDUCED CELL-DEATH; NITRIC-OXIDE; NATURAL-RESISTANCE; BCL-2 EXPRESSION; DOWN-REGULATION; INTRACELLULAR PARASITES; ALVEOLAR MACROPHAGES; PROTECTS MACROPHAGES;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
74
Recensione:
Indirizzi per estratti:
Indirizzo: Garcia, LF UnivrAntioquia, Fac Med, Ctr Invest Med, Lab Cent Invest,Grp Inmunol Celula Univ Antioquia Medellin Colombia t Invest,Grp Inmunol Celula
Citazione:
M. Rojas et al., "TNF-alpha and IL-10 modulate the induction of apoptosis by virulent Mycobacterium tuberculosis in murine macrophages", J IMMUNOL, 162(10), 1999, pp. 6122-6131

Abstract

The Bcg/Nramp1 gene controls early resistance and susceptibility of macrophages to mycobacterial infections. We previously reported that Mycobacterium tuberculosis-infected (Mtb) B10R (Bcg(r)) and BIOS (Bcg(s)) macrophages differentially produce nitric oxide (NO-), leading to macrophage apoptosis, Since TNF-alpha and IL-10 have opposite effects on many macrophage functions, we determined the number of cells producing TNF-alpha and IL-10 in Mtb-infected or purified protein derivative-stimulated B10R and B10S macrophageslines, and Nramp1(+/+) and Nramp1(-/-) peritoneal macrophages and correlated them with Mtb-mediated apoptosis, Mtb infection and purified protein derivative treatment induced more TNF-alpha(+)Nramp1(+/+) and B10R, and more IL-10(+)Nramp1(-/-) and B10S cells, Treatment with mannosylated lipoarabinomannan, which rescues macrophages from Mtb-induced apoptosis, augmented the number of IL-10 B10R(+) cells, Anti-TNF-alpha inhibited apoptosis, diminished NO- production, p53, and caspase 1 activation and increased Bcl-2 expression. In contrast, anti-IL-10 increased caspase 1 activation, p53 expression, and apoptosis, although there was no increment in NO- production. MurinerTNF-alpha induced apoptosis in noninfected B10R and B10S macrophages thatwas reversed by murine rIL-10 in a dose-dependent manner with concomitant inhibition of NO- production and caspase 1 activation. NO- and caspase 1 seem to be independently activated in that aminoguanidine did not affect caspase 1 activation and the inhibitor of caspase 1, Tyr-Val-Ala-Asp-acylooxymethylketone, did not block NO- production; however, both treatments inhibited apoptosis, These results show that Mtb activates TNF-alpha- and IL-10-dependent opposite signals in the induction of macrophage apoptosis and suggest that the TNF-alpha-IL-10 ratio is controlled by the Nramp1 background of resistance/susceptibility and may account for the balance between apoptosisand macrophage survival.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 04/12/20 alle ore 06:04:02