Galectina-3 (Gal-3) exerce papel chave no controle de etapas iniciais e tardias da infecção por Toxoplasma gondii em células trofoblásticas humanas e vilos placentários

Abstract

Galectin-3 (Gal-3) is a lectin that binds to β-galactosides, expressed in cells of the placental microenvironment. This lectin is involved in various biological processes, such as modulation of the immune system and control of parasitic infections, including those caused by Toxoplasma gondii. This infection can lead to congenital transmission, causing spontaneous abortions, prematurity, and fetal abnormalities. However, little is known about the role of Gal-3 in T. gondii infection at the maternal-fetal interface. This study aimed to investigate the role of Gal-3 in T. gondii infection in the gestational context. To this end, we promoted the knockdown of Gal-3 expression using RNA interference (RNAi) in BeWo cells. In placental villous explants, we used β-lactose or the synthetic inhibitor GB1107. We showed that decreased Gal-3 expression in BeWo cells increases T. gondii invasion and proliferation and negatively regulates MIF and IL-6 levels. Similar results were observed in placental villi treated with the synthetic inhibitor, highlighting the role of this lectin in modulating the immune response. On the other hand, blocking Gal-3 with β-lactose led to control of the parasitic infection. Collectively, our study reveals Gal-3 as a promising target protein in the context of congenital toxoplasmosis.