TNF receptor p55 signaling modulates Il-12/23p40 production in Yersinia enterocolitica-induced reactive arthritis.

MAYORDOMO AC ; JERÉZ MB; ARIAS JL; SILVA JE,; CARGNELUTTI E,; GORLINO C, ; DI GENARO MS

Buenos Aires

Congreso; LXIII Reunión Anual de SAI en el marco del Primer Congreso Internacional conjunto (I Meeting LASID-SAI-FAIC) junto a LASID (IV Meeting LASID) y FAIC(FAIC-II); 2015

Sociedad Argentina de Inmunlogia

Background: TNFRp55 deficient (TNFRp55-/-) mice develop reactive arthritis (ReA) after Yersinia enterocolitica (Ye) O:3 infection. Heightened IL-12/23p40 production was detected. The mechanism of this deregulation has not been clarified. The purpose was to gain insight into a regulatory role of TNFRp55 signaling on IL-12/23p40 production in Ye-induced ReA.Methods: Wild-type (WT) and TNFRp55-/- mice (C57BL/6) were infected orogastrically with Ye (1-5 x 108 CFU). At day 14 after infection (arthritis onset), splenocytes (2 x 106 cell/well) were stimulated with LPS (1 ug/ml). Inhibitors of p38 (SB203580), ERK (PD98059) or JNK (SP600125) MAPKs were added. IL-12/23p40 and IFN-g in the supernatants were determined by ELISA. The response was compared with LPS-stimulated naïve splenocytes.Results: At 24h after LPS stimulation, splenocytes from Ye-infected WT mice were more susceptible to inhibition of IL-12/23p40 production and to induction of IL-10 than naïve cells (p