CIBICI   14215
CENTRO DE INVESTIGACION EN BIOQUIMICA CLINICA E INMUNOLOGIA
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
IL-6 drives cardiac macrophage profile and regulates the lethal release of Nitric Oxide production through IL-1β inhibition during parasite infection
Autor/es:
SANMARCO, LM; PONCE, NE; VISCONTI, LM; EBERHARDT, N; SPITALE, NB; BERNARDI, GA; MINGUEZ, RA; AOKI, MP
Reunión:
Jornada; LXIII Reunión Anual de la Sociedad Argentina de Inmunología; 2015
Resumen:
Monocytes/Macrophages are a heterogeneous populationof immune cells that have a range of roles in both the induction and resolutionof inflammation. The production of nitric oxide (NO) is associated with thekilling of microorganisms and characterizes M1-type macrophage response whereasthe expression of arginase is associated with repair and characterizes M2-typemacrophage response. The factors involved in cardiac macrophage profiledifferentiation during T. cruzi infectionhave not been characterized. The aim of the present work was to study theeffect of IL-6 in soluble mediators production, kinetic of cardiac macrophage subsetsand the crosstalk between monocytes/macrophages and myocardium during T.cruzi infection. We observed that,while at 4 days post-infection (dpi) C57BL/6 mice (WT) exhibited higher levelsof cardiac M1 (F4/80+CD86+CD206-) than M2 macrophages (F4/80+CD86-CD206+)(p<0.05), later the macrophage populations were biased to sustained M2subset. Moreover, IL6KO mice exhibited a late M1 profile (14 dpi) (p<0.001) withlower cardiac parasite burden at 21 dpi (p<0.001). Concomitantly, weobserved a dramatic increased of NO levels in serum of deficient animals at 4 and19 dpi (p<0.001 and p<0.05) compared with WT. To support these results,we showed that mice and human macrophages stimulated with IL-6 recombinantbioactive produced lower levels of NO (p<0.05). These results suggest thatIL-6 would have a key role in regulating the production of NO and exhibit theimportance of knowing the pleiotropic effect of IL-6, given the fact that this cytokine is atherapeutic target in many diseases.