IIFP   25103
INSTITUTO DE ESTUDIOS INMUNOLOGICOS Y FISIOPATOLOGICOS
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
Interleukin (IL)-17AA Reduces Pro-Inflammatory Cytokine Production By Inflammatory Bowel Disease Mucosa Cultured Ex Vivo.
Autor/es:
RENATA CURCIARELLO; PAOLO BIANCHERI; ANDRÉS ROCCA; ALICIA SAMBUELLI; GUSTAVO J. CORREA; MARTÍN YANTORNO; NÉSTOR CHOPITA; THOMAS T, MACDONALD; GUILLERMO, DOCENA
Lugar:
Medellín
Reunión:
Congreso; IMMUNOCOLOMBIA 2015. 11th Congress of the Latin American Association of Immunology-ALAI, 10th Colombian Congress of Allergy Asthma and Immunology; 2015
Institución organizadora:
ALAI
Resumen:
Inflammatory bowel disease (IBD) are chronic disorders in which pro-inflammatory cytokinesplay a key role in the immunopathogenesis. Interleukin (IL)-17A was found to be up-regulatedin mucosal lesions from IBD patients. IL-17 cytokines family includes 5 members (IL-17A/F/E/C and D), which constitute dimers in their active form. IL-17A shares 50% homologywith IL-17F, they may form IL-17AA and IL-17FF homodimers or IL-17A/F heterodimers.Since the role of IL-17 dimers is unknown in IBD, we studied the pro-inflammatory effect ofIL-17AA, IL-17FF and IL-17-A/F in intestinal samples of ulcerative colitis (UC) and Crohn?sdisease (CD) patients. Inflamed colonic biopsies from 26 IBD patients (13 UC and 13 CD) werecultured ex vivo for 24 hours with IL-17AA, IL-17FF or IL-17A/F (1 ng/ml). Mucosalmyofibroblasts isolated from the inflamed colon of 4 CD and 4 UC patients were cultured withincreasing concentrations (1-100 ng/ml) of each dimer or tumor necrosis factor (TNF)-alpha (20ng/ml) as control. IL-6 and IL-8 were measured in culture supernatants by ELISA. We found ininflamed IBD biopsies that IL-17AA, but not IL-17FF, significantly reduced both IL-6 and IL-8production, whereas IL-17A/F only decreased IL-8 release. As expected, TNF-alpha stimulationsignificantly increased IL-6 and IL-8 production in CD and UC myofibroblasts. However,neither IL-17AA, nor IL-17FF, nor IL-17A/F modified the secretion of IL-6 and IL-8 in IBDmyofibroblasts at these tested concentrations. In conclusion, we found that IL-17AA exerted ananti-inflammatory action on inflamed IBD biopsies, and this effect would not be directlymediated by myofibroblasts. Further studies are needed to identify the cell target for IL-17AAin IBD mucosa.