Human neural angiostrongyliasis is an emerging infectious disease caused by nematode Angiostrongylus cantonensis. The present study investigated the presence of Angiostrongylus spp. in terrestrial molluscs collected from the following areas in the Metropolitan Region of Aracaju, Sergipe State, Brazil: Barra dos Coqueiros, Nossa Senhora do Socorro, Sao Cristovao and Aracaju. In total, 703 specimens representing 13 mollusc species were screened for Angiostrongylus spp. Larvae of Angiostrongylus spp. were found in three species. Larvae recovered from Achatina fulica were used for experimental infection in Wistar rats (Rattus norvegicus). For specific identification of nematodes, the mitochondrial cytochrome c oxidase subunit I (COI) was sequenced from both larvae and adults recovered from molluscs and rats, respectively. Infection with A. cantonensis was detected in all municipalities and in the following three host species: Bulimulus tenuissimus, Cyclodontina fasciata (Barra dos Coqueiros), and A. fulica (Aracaju, Nossa Senhora do Socorro and Sao Cristovao). Co-infections were also found with Caenorhabditis sp. and Strongyluris sp. larvae. This is the first study of the helminth fauna associated with the terrestrial malacofauna in Sergipe State, and confirms that these three snail species are involved in the transmission of A. cantonensis in the state. In addition, B. tenuissimus and C. fasciata are newly reported natural hosts of the parasite.

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Chagas disease, caused by the parasite Trypanosoma cruzi, is considered endemic in more than 20 countries but lacks both an approved vaccine and limited treatment for its chronic stage. Chronic infection is most harmful to human health because of long-term parasitic infection of the heart. Here we show that immunization with a virus-like particle vaccine displaying a high density of the immunogenic α-Gal trisaccharide (Qβ-αGal) induced several beneficial effects concerning acute and chronic T. cruzi infection in α1,3-galactosyltransferase knockout mice. Approximately 60% of these animals were protected from initial infection with high parasite loads. Vaccinated animals also produced high anti-αGal IgG antibody titers, improved IFN-γ and IL-12 cytokine production, and controlled parasitemia in the acute phase at 8 days post-infection (dpi) for the Y strain and 22 dpi for the Colombian strain. In the chronic stage of infection (36 and 190 dpi, respectively), all of the vaccinated group survived, showing significantly decreased heart inflammation and clearance of amastigote nests from the heart tissue.

Human ascariasis is the most prevalent but neglected tropical disease in the world, affecting approximately 450 million people. The initial phase of Ascaris infection is marked by larval migration from the host’s organs, causing mechanical injuries followed by an intense local inflammatory response, which is characterized mainly by neutrophil and eosinophil infiltration, especially in the lungs. During the pulmonary phase, the lesions induced by larval migration and excessive immune responses contribute to tissue remodeling marked by fibrosis and lung dysfunction. In this study, we investigated the relationship between SIgA levels and eosinophils. We found that TLR2 and TLR4 signaling induces eosinophils and promotes SIgA production during Ascaris suum infection. Therefore, control of parasite burden during the pulmonary phase of ascariasis involves eosinophil influx and subsequent promotion of SIgA levels. In addition, we also demonstrate that eosinophils also participate in the process of tissue remodeling after lung injury caused by larval migration, contributing to pulmonary fibrosis and dysfunction in re-infected mice. In conclusion, we postulate that eosinophils play a central role in mediating host innate and humoral immune responses by controlling parasite burden, tissue inflammation, and remodeling during Ascaris suum infection. Furthermore, we suggest that the use of probiotics can induce eosinophilia and SIgA production and contribute to controlling parasite burden and morbidity of helminthic diseases with pulmonary cycles.

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The development of vaccines for human leishmaniasis is one of the most important approaches for effectively controlling and/or eradicating the several forms of the disease. Based on the knowledge obtained from the practice of leishmanization and its protective immune response, several strategies have been used to develop vaccines against Leishmania species, such as the use of whole killed and attenuated parasites, recombinant proteins, and DNA vaccines. An ideal vaccine should be safe, effective, and immunogenic. Although several candidates have achieved safety and some level of effectiveness, the current challenge in the development of prophylactic vaccines is to achieve long-lasting immune protection by generating a robust and irreversible Th1 adaptive immune response in the host, with rapid recruitment of memory and effectors T cells at key acute points of infection. However, despite all efforts over the years, due to the antigenic diversity of the parasite and the complexity of the host’s immune response, human vaccine trials have been disappointing in mediating long-term immunity against sandfly-delivered infection. Therefore, more investments in this field should be carried out to translate preclinical findings from mice to humans through effective vaccine development strategies.

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