INVESTIGADORES
GOLDMAN Alejandra
congresos y reuniones científicas
Título:
TOXOPLASMA GONDII INFECTION MODULATES SYSTEMIC ALLERGIC IMMUNE RESPONSE
Autor/es:
FENOY I. ; SANCHEZ V. ; SOTO A. ; PICCHIO M. ; PERRONE SIBILIA M. ; ALDIRICO M. ; MARTIN V. ; GOLDMAN A
Reunión:
Congreso; LXII Reunión Anual de la Sociedad Argentina de Inmunología; 2014
Resumen:
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<0.05, **p<0.01 y ***p<0.001
vs O group, ANOVA with Bonferroni?s test a posteriori). Direct cutaneous
anaphylaxis was next assayed. Infection before allergic sensitization
diminished the anaphylactic reaction, indicating that
mice in both TO groups show lower
vasodilatation and vascular permeability due to lower cutaneous mast cell
degranulation. Our results extend earlier work and show that, in addition to
lung airway inflammation, T. gondii infection can suppress allergic
responses at systemic level. These results open the possibility that this
protozoan infection could modulate other allergic disorders such as atopic
dermatitis or oral allergies.