Toxoplasma gondii chronic infection modulates the first stages of atopic dermatitis sensitization

M PERRONE SIBILIA; MA ALDIRICO; M PICCHIO; V SANCHEZ; N ARCON; GUIDO RATTAY; R MORETTA; V MARTÍN; I FENOY; A GOLDMAN

Congreso; LXVI Reunión Anual de la Sociedad Argentina de Inmunología 2018; 2018

We previously showedthat chronic T. gondii infection diminishes the susceptibility to developatopic dermatitis by using amurine experimental model with OVA as allergen. Skin histopathology of miceinfected before allergic sensitization was similar to normal mice. Diminished OVAspecific IgE and IgG1 levels and reduced systemic and local Th1/Th2 cytokineswere detected. These results suggested that regulatory cells induced by theparasite may account for the immunomodulatory effect. However, no significantdifferences were observed in regulatory cytokine production or CD4+Foxp3+T cells between groups. Based on theseresults, we hypothesized that the parasite could modulate the allergicsensitization by regulating the innate immune response. Therefore, the aim ofthe present work was to study the first stages of the sensitization process. AdultBALB/c mice chronically infected with T.gondii cysts were epicutaneously sensitized with OVA (TDA) and euthanizedat 0, 2, 6 or 24hs later. Non-infected mice sensitized with OVA (DA) where usedas control. Systemic cytokinelevels were analyzed in splenocytes exvivo stimulated with PMA/ionomycin. T.gondii infected mice showed decreased IL-4 (TDA=89.3±31.6//DA=523±41.7), IL-5(TDA=42.2±23.4//DA=329.3±43.8) and augmented IFN-g levels (TDA=2961±474.7//DA=1660±134.6) compared to control mice at 24hs(p