Toxoplasma gondii chronic infection prevents the development of atopic dermatitis

MATÍAS DAMIÁN PERRONE SIBILIA; MARÍA DE LOS ÁNGELES ALDIRICO; ARIADNA SOTO; MARIANO SERGIO PICCHIO; VANESA ROXANA SÁNCHEZ; NADIA ARCON; FLORENCIA MAGALÍ GIORGIO; VALENTINA MARTIN; SILVIA VANZULLI; IGNACIO FENOY; ALEJANDRA GOLDMAN

Congreso; Recunión Anual de la Sociedad Argentina de Inmunología; 2016

SAI

We previously showed that T. gondii infection diminishes the susceptibility to develop experimental asthma. The parasite immunomodulatory ability extends to systemic level. Hence, these results suggested that this protozoan infection could modulate other allergic disorders. The aim of the present work was to study whether T. gondii infection also modulates the development of atopic dermatitis. One month before allergic sensitization, adult BALB/c mice were orally infected with T. gondii cysts. Mice were epicutaneous sensitized with OVA (TDA) or PBS (T). Treatment was repeated twice with a 2-week resting period between each sensitization. Controls include non-infected mice sensitized with OVA (DA) and non-infected mice treated with PBS (N). The analysis was performed one day after the last week of sensitization. Skin and blood samples were collected to evaluate histopathology, and OVA-specific IgE, IgG1 and IgG2a antibodies respectively. Ex vivo stimulation of splenocytes with OVA was performed and supernatant IL-4, IL-5 and IFN- cytokine levels were evaluated. Allergic mice showed pathological changes characteristic of atopic dermatitis, compared with normal mice. These changes include epidermal hyperplasia, hyperkeratosis and infiltration of inflammatory cells in the dermis and epidermis. Mice infected with T. gondii before allergic sensitization showed a histopathology similar to normal mice, with no epidermal hyperplasia, orthokeratosis and poor inflammatory infiltrate in the dermis and epidermis. A trend to decreased OVA-specific IgE and significant diminished IgG1 levels in TDA compared to the DA group were detected (p