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Titolo:
HELICOBACTER-HEPATICUS TRIGGERS COLITIS IN SPECIFIC-PATHOGEN-FREE INTERLEUKIN-10 (IL-10)-DEFICIENT MICE THROUGH AN IL-12- AND GAMMA-INTERFERON-DEPENDENT MECHANISM
Autore:
KULLBERG MC; WARD JM; GORELICK PL; CASPAR P; HIENY S; CHEEVER A; JANKOVIC D; SHER A;
Indirizzi:
NIAID,PARASIT DIS LAB,IMMUNOBIOL SECT,NIH,BLDG 4,ROOM 126,CTR DR MSC 0425 BETHESDA MD 20892 NCI,VET & TUMOR PATHOL SECT,ANIM SCI BRANCH,OFF LAB ANIM RESOURCES,DIV BASIC SCI BETHESDA MD 20892 NCI,FREDERICK CANC RES & DEV CTR,ANIM HLTH DIAGNOST LAB,LAB ANIM SCI PROGRAM,SCI APPLICAT CORP FREDERICK MD 21702 BIOMED RES INST ROCKVILLE MD 20852
Titolo Testata:
Infection and immunity (Print)
fascicolo: 11, volume: 66, anno: 1998,
pagine: 5157 - 5166
SICI:
0019-9567(1998)66:11<5157:HTCISI>2.0.ZU;2-6
Fonte:
ISI
Lingua:
ENG
Soggetto:
CD4(+) T-CELLS; INFLAMMATORY BOWEL-DISEASE; CHRONIC INTESTINAL INFLAMMATION; CHRONIC ACTIVE HEPATITIS; MONOCLONAL-ANTIBODIES; BACTERIAL-INFECTION; ULCERATIVE-COLITIS; MUTANT MICE; SCID MICE; CYTOKINE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
41
Recensione:
Indirizzi per estratti:
Citazione:
M.C. Kullberg et al., "HELICOBACTER-HEPATICUS TRIGGERS COLITIS IN SPECIFIC-PATHOGEN-FREE INTERLEUKIN-10 (IL-10)-DEFICIENT MICE THROUGH AN IL-12- AND GAMMA-INTERFERON-DEPENDENT MECHANISM", Infection and immunity (Print), 66(11), 1998, pp. 5157-5166

Abstract

Mice rendered deficient in interleukin-10 (IL-10) by gene targeting (IL-10(-/-) mice) develop chronic enterocolitis resembling human inflammatory bowel disease (IBD) when maintained in conventional animal facilities. However, they display a minimal and delayed intestinal inflammatory response when reared under specific-pathogen-free (SPF) conditions, suggesting the involvement of a microbial component in pathogenesis. We show here that experimental infection with a single bacterial agent, Helicobacter hepaticus, induces chronic colitis in SPF-reared IL-10(-/-) mice and that the disease is accompanied by a type 1 cytokine response (gamma interferon [IFN-gamma], tumor necrosis factor alpha, and nitric oxide) detected by restimulation of spleen and mesenteric lymph node cells with a soluble H. hepaticus antigen (Ag) preparation. In contrast, wild-type (WT) animals infected with the same bacteria didnot develop disease and produced IL-10 as the dominant cytokine in response to Helicobacter Ag. Strong H. hepaticus-reactive antibody responses as measured by Ag-specific total immunoglobulin G (IgG), IgG1, IgG2a, IgG2b, IgG3, and IgA were observed in both WT and IL-10(-/-) mice. In vivo neutralization of IFN-gamma or IL-12 resulted in a significant reduction of intestinal inflammation in H. hepaticus-infected IL-10(-/-) mice, suggesting an important role for these cytokines in the development of colitis in the model. Taken together, these microbial reconstitution experiments formally establish that a defined bacterial agent can serve as the immunological target in the development of large bowel inflammation in IL-10(-/-) mice and argue that in nonimmunocompromised hosts IL-10 stimulated in response to intestinal flora is important in preventing IBD.

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Documento generato il 27/10/20 alle ore 05:33:21