info:eu-repo/semantics/article
Chronic infection with the protozoan Toxoplasma gondii prevents the development of experimental atopic dermatitis in mice
Fecha
2019-11-02Registro en:
Perrone Sibilia, Matías Damián; Aldirico, María de Los Ángeles; Soto, Ariadna Soledad; Picchio, Mariano Sergio; Sánchez, Vanesa Roxana; et al.; Chronic infection with the protozoan Toxoplasma gondii prevents the development of experimental atopic dermatitis in mice; Elsevier Ireland; Journal of Dermatological Science; 96; 3; 2-11-2019; 143-150
0923-1811
1873-569X
CONICET Digital
CONICET
Autor
Perrone Sibilia, Matías Damián
Aldirico, María de Los Ángeles
Soto, Ariadna Soledad
Picchio, Mariano Sergio
Sánchez, Vanesa Roxana
Arcon, Nadia
Moretta, Rosalia Ester
Martín, Valentina
Vanzulli, Silvia
Fenoy, Ignacio Martín
Goldman, Alejandra
Resumen
Background: Supporting the hypothesis thatT. gondii infection protects against allergy in humans we previously demonstrated that this infection can modulate not only the susceptibility to develop respiratory allergies in mice but also suppresses allergic responses at systemic level. This latter finding suggests that T. gondii infection could prevent the onset of other allergic diseases, such as atopic dermatitis. At present, few studies have investigated the modulation of atopic dermatitis by parasite infections. Objective: Here, we sought to investigate whether chronic infection with T. gondii is capable of modulating the development of atopic dermatitis. Methods: Chronically infected mice were sensitized by repeated epicutaneous ovalbumin administration. Skin histopathology, humoral response, cytokine production and innate type-II lymphoid cells (ILC2) were assessed. Results: A marked reduction in epidermal thickness and dermal inflammatory infiltrate along with a reduction in mast cell count was observed in infected mice compared to non-infected mice. These results correlated with a diminished TH2 and TH1 allergen specific response. Reduced type-II IL-4 and IL-5 cytokines were already detected during the first 24 h of allergen sensitization in splenocytes and draining lymph nodes from infected mice. Moreover, this reduced type-II profile in chronically infected animals correlated with diminished ILC2 number in draining lymph nodes. Conclusion: Chronic infection withT. gondii prevents the development of atopic dermatitis. The diminished susceptibility seems to result from changes in type-II innate immune response that may lead to the induction of a deficient TH2 response and consequently to a lower susceptibility to develop atopic dermatitis.