Toxoplasma gondii infection modulates systemic allergic immune response

FENOY IGNACIO; VANESA R. SÁNCHEZA; ARIADNA SOTO; MARIANO PICCHIO; MATIAS PERRONE; MARÍA DE LOS ANGELES ALDIRICO; VALENTINA MARTIN; ALEJANDRA GOLDMAN

Congreso; LXII REUNIÓN ANUAL Sociedad Argentina de Inmunología; 2014

In agreement with epidemiological studies, we previously showed that T. gondii infection prevents allergic airway inflammation. The mechanisms would be related to the strong Th1 response induced against the parasite and to regulatory cells induction. The aim of the present study is to analyze whether T. gondii allergy modulation extents to a systemic level or it is only confined to the lung. BALB/c mice were orally infected by T. gondii cysts. Acute and chronic infected animals were ip sensitized with the allergen (OVA)/alum and one week later mice were aerosols challenge (TOa and TOc respectively). Control groups include naive, acute and chronic infected mice (N, Ta y Tc) as negative control and allergic mice (OVA-sensitized and challenged) as positive control (O). Splenocytes were ex vivo cultured and OVA stimulated to evaluate cytokine production and proliferative capacity. Infection before allergic sensitization resulted in a diminished in Th2 cytokines (IL-4: N 4±3, Ta 27±15, Tc 3±1, O 393±98, TOa 192±38*, TOc 21±7**; IL-5: N 50±31, Ta 7±2, Tc 10±10, O 503±173, TOa 110±55*, TOc 89±50*; IFN-γ: N 52±13, Ta 52±16, Tc 20±3, O 72±24, TOa 257±92*, TOc 40±21; pg/ml±SEM) and it also resulted in a lower proliferative capacity (N 2673±570, Ta 3876±947, Tc 2580±400, O 12892±1650, TOa 1310±427***, TOc 1794±358***; ΔCPM±SEM) (*p