Insights into the Role of Proteolytic and Adhesive Domains of Snake Venom Metalloproteinases from spp. in the Control of Infection.

Toxoplasmosis is an alarming public health problem that affects more than one-third of the world's population. In our work, we investigated the antiparasitic effects of catalytically active [BpMP-I and Jararhagin (Jar)] and catalytically inactive [Jararhagin-C (Jar-C)] snake venom metalloproteinases (SVMPs) in human HeLa cells. These toxins impaired the parasite invasion and intracellular growth, and modulated IL-6, IL-8, and MIF cytokines that control the cell susceptibility and response against .

Taenia crassiceps cysticerci antigenic extract controls Toxoplasma gondii proliferation in human trophoblast cells and upregulates IL-10 production.

Neglected tropical diseases caused by helminths such as strongyloidiasis and those caused by protozoa such as toxoplasmosis are public health problems, especially in poorer countries. Considering that helminthic infections can alter susceptibility to other parasites, it is important to study the impact of this interaction in different scenarios/models, such as the maternal-fetal interface. This research aims to evaluate the role of saline extract (SE) of Taenia crassiceps cysticerci during Toxoplasma gondii infection in human villous trophoblastic cells of the BeWo lineage.

Galectin-3 plays a key role in controlling infection by in human trophoblast cells and human villous explants.

Galectin-3 (Gal-3) is a β-galactoside-binding lectin 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 illness. infection can lead to congenital transmission and cause miscarriages, prematurity and fetal anomalies.

Copaifera spp. oleoresins control Trypanosoma cruzi infection in human trophoblast cells (BeWo) and placental explants.

Congenital Chagas disease (CCD) is a worldwide neglected problem with significant treatment limitations. This study aimed to evaluate the potential of Copaifera spp. oleoresins (ORs) against Trypanosoma cruzi infection in trophoblast cells (BeWo lineage) and human chorionic villous explants (HCVE).

P21 recombinant protein modulates infection in different experimental models of the human maternal-fetal interface.

Introduction: is the etiologic agent of toxoplasmosis, a disease that affects about one-third of the human population. Most infected individuals are asymptomatic, but severe cases can occur such as in congenital transmission, which can be aggravated in individuals infected with other pathogens, such as HIV-positive pregnant women. However, it is unknown whether infection by other pathogens, such as , the etiologic agent of Chagas disease, as well as one of its proteins, P21, could aggravate infection.

Rottlerin impairs early and late steps of Toxoplasma gondii infection in human trophoblast cells and villous explants.

Congenital toxoplasmosis, caused by the opportunistic protozoan parasite T. gondii, can cause stillbirths, miscarriages and fetal abnormalities, as well as encephalitis and chorioretinitis in newborns. Available treatment options rely on antiparasitic drugs that have been linked to serious side effects, high toxicity and the development of drug-resistant parasites.

LPS-mediated activation of TLR4 controls Toxoplasma gondii growth in human trophoblast cell (BeWo) and human villous explants in a dependent-manner of TRIF, MyD88, NF-κB and cytokines.

We evaluated the influence of the Toll-like receptor (TLR)-4 pathways on BeWo, JEG-3 and HTR-8/SVneo cells, as well as in human villous explants infected with Toxoplasma gondii. Cells and explants were stimulated with LPS for 24 or 48 h and processed for the MTT assay, and expression of TLR4 was evaluated by confocal microscopy. In addition, we used peptides that inhibit MyD88 or TRIF, and inhibitor to NF-κB.

Biogenic Silver Nanoparticles Can Control Infection in Both Human Trophoblast Cells and Villous Explants.

The combination of sulfadiazine and pyrimethamine plus folinic acid is the conventional treatment for congenital toxoplasmosis. However, this classical treatment presents teratogenic effects and bone marrow suppression. In this sense, new therapeutic strategies are necessary to reduce these effects and improve the control of infection.