INVESTIGADORES
MARTIN Valentina
congresos y reuniones científicas
Título:
ACUTE TOXOPLASMA GONDII INFECTION BLOCKS THE DEVELOPMENT OF ALLERGIC LUNG INFLAMMATION VIA REGULATORY CELLS INDUCTION
Autor/es:
IGNACIO FENOY ; VANESA SANCHEZ; MARIANA ARGENZIANO; ARIADNA SOTO; MARIANO PICCHIO; FLORENCIA MARCH; FACUNDO CASTERA; ANDREA MAGLIOCO ; VALENTINA MARTIN; ALEJANDRA GOLDMAN
Reunión:
Congreso; LXi Reunión Anual de la Sociedad Argentina de Inmunología; 2013
Resumen:
We have previously shown that T.gondii infection prevents allergic airway inflammation. Thoracic lymph nodecells (TLNC) from acute infected and sensitized mice (TO) show a decrease in antigen (OVA)-specific T cellproliferation compared to allergic mice (O). The presence of regulatory cells is among the possibilities thatcould explain these results. Hence, we studied the ability of TLNC from TO or only T. gondii infected (T) miceto suppress T cell proliferation. TLNC from O mice were co-cultivated with TLNC from T, TO or naïve mice (N)and stimulated with OVA. TO cells inhibited T cell proliferation (N:37±7, T:11±4, TO:7±2*; SI±SEM). To assesswhether the suppressor activity was cell-cell contact dependent, conditioned medium from cultures from TO,T or N TLNC stimulated for 4 days with OVA was added to TLNC from O. Supernatant from TO TLNC was able to diminish OVA-specific proliferation (N:21±4, T:19±6, TO:8±3*; SI±SEM). To evaluate whether TLNC from TO can suppress an allergic lung inflammation, we adoptively transferred cells from N, T and TO groups to OVAsensitized mice which had received two OVA/Al ip injections. One day later, receptor mice were aerosol challenged with OVA for three consecutive days. Animals transferred with TO TLNC had significantly less bronchoalveolar eosinophilia (N:42±7; T:22±4; TO:18±7*; %±SEM) and a significant reduction in lung mucus production (N:0,93±0,23; T:0,39±0,22; TO:0,15±0,08*; index±SEM). Experiments with IL-10 KO mice showed that this cytokine doesn?t play a role in the supression. Voisin et. al. (Infect Immun 2004) described, in lung from infected mice, a NO dependent supression. We assessed lung iNOS expression by RT-qPCR. TO mice showed increased expression versus N and O groups (N:1,1±0,1; T:2,9±0,7; O:0,53±0,1; OT:4±0,8*; RU±SEM). All together, these data suggest that supression would be mediated by the induction of regulatory cells acting in a contact independent manner.*p<0,05 TO vs. N Kruskal-Wallis Dunn a posteriori