Papel de CCR5 nas alterações morfológicas no intestino delgado durante a infecção oral aguda por Toxoplasma gondii em modelos murinos

Abstract

Toxoplasma gondii is the etiological agent of toxoplasmosis and this parasite induces mainly a type 1 immune response. It has already been known that the expression of the CCR5 chemokine receptor is important for the cell recruitment in T. gondii infection, being important for the immune control of acute infection. In addition, it was found that genetically deficient animals for this receptor are more susceptible to infection and have higher parasite load. However, morphological changes in the small intestine, the main entry site of the parasite, in the absence of the receptor, require further investigation. To this end, animals genetically deficient in CCR5 (CCR5-/-) and control animals, C57BL/6, were infected orally and the morbidity, survival and intestinal histological parameters were evaluated. CCR5-/- animals were more susceptible to infection than control animals. Infection by the parasite induced a mild inflammation in the small intestine at day 5 of infection, and C57BL/6 showed an increase in the number of Paneth cells and CCR5-/- animals an increase in the number of intraepithelial lymphocytes. However, increased inflammatory changes were observed at day 7 of infection. The inflammatory changes were more pronounced in CCR5-/- animals. In addition, a decrease in number of goblet cells, Paneth and intraepithelial lymphocytes in the small intestine was observed in mice of both lineages, which were higher in CCR5-/- animals. In conclusion, the CCR5 chemokine receptor is involved in protecting against tissue lesions by T. gondii infection in the small intestine.