Galectin-1 (Gal-1), an endogenous glycan-binding protein, is widely distributed at sites of inflammation and microbial invasion. Despite considerable progress regarding the immunoregulatory activity of this lectin, the role of endogenous Gal-1 during acute parasite infections is uncertain. In this study, we show that Gal-1 functions as a negative regulator to limit host-protective immunity following intradermal infection with Trypanosoma cruzi. Concomitant with the upregulation of immune inhibitory mediators, including IL-10, TGF-β1, IDO, and programmed death ligand 2, T. cruzi infection induced an early increase of Gal-1 expression in vivo. Compared to their wild-type (WT) counterpart, Gal-1–deficient (Lgals1−/−) mice exhibited reduced mortality and lower parasite load in muscle tissue. Resistance of Lgals1−/− mice to T. cruzi infection was associated with a failure in the activation of Gal-1–driven tolerogenic circuits, otherwise orchestrated by WT dendritic cells, leading to secondary dysfunction in the induction of CD4+CD25+Foxp3+ regulatory T cells. This effect was accompanied by an increased number of CD8+ T cells and higher frequency of IFN-γ–producing CD4+ T cells in muscle tissues and draining lymph nodes as well as reduced parasite burden in heart and hindlimb skeletal muscle. Moreover, dendritic cells lacking Gal-1 interrupted the Gal-1–mediated tolerogenic circuit and reinforced T cell–dependent anti-parasite immunity when adoptively transferred into WT mice. Thus, endogenous Gal-1 may influence T. cruzi infection by fueling tolerogenic circuits that hinder anti-parasite immunity.
A test based on the inhibition by antibodies of the trans-sialidase was used to analyze infection by Trypanosoma cruzi, the agent of Chagas' disease. Sera collected during the longitudinal follow-up of benznidazole-treated acutely and congenitally infected patients became negative for T. cruzi as determined by tests presently used to assess cure; however, the sera remained positive for T. cruzi by the trans-sialidase inhibition assay (TIA) up to 14 years after treatment. Therefore, TIA is a highly sensitive marker for previous T. cruzi infection.
Strongyloides stercoralis chronic infections are usually asymptomatic and underestimated. We used direct fresh stool examination, Ritchie's method, and agar plate culture for diagnosis in patients with eosinophilia and previous residence in endemic areas. The frequency of strongyloidosis detected among these patients was high: 21 of 42 were positive. Among them, 10 were positive only by agar plate culture. After ivermectin treatment, patients resulted negative for parasitological tests and reduced their eosinophil counts. Half of the submitted patients that were followed 4–12 months after treatment remained negative without eosinophilia, except one who showed an eosinophil ascending curve before reappearance of larvae in stools. The high frequency of strongyloidosis found in this group emphasizes the relevance of including this parasitosis among differential diagnosis in patients with eosinophilia and past risk of S. stercoralis infection to prevent disseminated infections secondary to corticoid therapy.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.