Ileal inflammation is reduced due to treatment with a metalloprotease from BmooMP-α-I snake venom in an experimental model of Toxoplasma gondii infection.

The selection process for advanced therapies in patients with inflammatory bowel diseases (IBDs) must prioritize safety, especially when considering new biologic agents or oral molecule modulators. In C57BL/6 mice, oral infection with Toxoplasma gondii induces intestinal inflammation through excessive tumor necrosis factor (TNF) production, making TNF neutralization a potential therapeutic intervention. Considering this, the present study aimed to evaluate the therapeutic effects of BmooMP-α-I, a snake venom metalloprotease isolated from Bothrops moojeni, which could promote TNF hydrolysis, in treating T.

A peptide originated from Toxoplasma gondii microneme 8 displaying serological evidence to differentiate recent from chronic human infection.

Toxoplasmosis is able to cause death and/or sequelae in foetuses from pregnant women and immunocompromised individuals. The early diagnosis, able to differentiate acute from chronic phases, is essential to define the treatment against this disease and minimize the risk of complications. Here we describe a peptide derived from microneme 8 (pMIC8) protein of Toxoplasma gondii, able to distinguish the phase of infection.

C57BL/6 mice immunized with synthetic peptides from Toxoplasma gondii surface and microneme immunodominant antigens are able to decrease parasite burden in the brain tissues.

Toxoplasmosis is a disease caused by Toxoplasma gondii, an intracellular protozoan able to infect a wide range of hosts. The infection is particularly severe in immunocompromised patients or during pregnancy, circumstances in which the parasite could find a more favorable microenvironment to replicate and invade host tissues. The current treatment consists in toxic drugs for the patients, being not appropriate for the fetuses and immunodeficient patients.

Astrocyte response to St. Louis encephalitis virus.

St. Louis encephalitis virus (SLEV), a flavivirus transmitted to humans by Culex mosquitoes, causes clinical symptoms ranging from acute febrile disorder to encephalitis. To reach the central nervous system (CNS) from circulating blood, the pathogen must cross the blood-brain barrier formed by endothelial cells and astrocytes.