Role of STAT1 and STAT6 molecules during toxocara canis infection (MPF1P.801)

Abstract

Abstract Toxocariasis is a worldwide zoonotic parasitic disease caused by Toxocara canis. Infection is caused by accidental ingestion of embryonated eggs, which hatch and the liberated larvae migrate to different organs. In murine models causes transitory hemorrhagic pulmonary lesions associated with strong TH2 responses and heavy parasite burdens. Alternatively activated macrophages (aaM), through STAT6 signaling, are involved in tissue repair, but its role in T. canis infection has not been determined yet. On the other hand, STAT1 has been clearly related to protection in protozoan infections, but its role on helminths is poorly known. Here we tried to recognize the role of STAT1 and 6 molecules in this infection by using STAT6-/- and STAT1-/- BALB/c mice in determining the outcome of experimental toxocariasis. Mice were infected, and specific antibodies, serum cytokines, parasite burden and lung pathology were analyzed at different times. STAT6+/+ and STAT1-/- mice displayed a Th2 immune response and their lung pathology were less evident compared to STAT6-/- mice, which displayed enhanced Th1 response but more damage in the lung. These differences in lung pathology were associated with the presence of aaM. In the other hand, parasite burden in STAT1-/- and STAT6-/- mice decreased as compared with wild type mice. Our data suggest that the absence of one or another response would contribute to eliminate this parasite, but the presence of aaM is necessary to control tissue damage.