Chronic infection with the protozoan Toxoplasma gondii prevents the development of experimental atopic dermatitis in mice

SIBILIA, MATÍAS DAMIÁN PERRONE; DE LOS ANGELES ALDIRICO, MARÍA; SOTO, ARIADNA SOLEDAD; PICCHIO, MARIANO SERGIO; SÁNCHEZ, VANESA ROXANA; ARCÓN, NADIA; MORETTA, ROSALÍA; MARTÍN, VALENTINA; VANZULLI, SILVIA; FENOY, IGNACIO MARTÍN; GOLDMAN, ALEJANDRA

JOURNAL OF DERMATOLOGICAL SCIENCE

ELSEVIER IRELAND LTD

Año: 2019

0923-1811

BackgroundSupporting 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.ObjectiveHere, we sought to investigate whether chronic infection with T. gondii is capable of modulating the development of atopic dermatitis.MethodsChronically infected mice were sensitized by repeated epicutaneous ovalbumin administration. Skin histopathology, humoral response, cytokine production and innate type-II lymphoid cells (ILC2) were assessed.ResultsA 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 hours 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.ConclusionChronic 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.