Publications by authors named "Julia Barbalho da Mota"
Genetic Ablation and Pharmacological Blockade of Bradykinin B1 Receptor Unveiled a Detrimental Role for the Kinin System in Chagas Disease Cardiomyopathy.
J Clin Med
April 2023
Chagas disease, the parasitic infection caused by , afflicts about 6 million people in Latin America. Here, we investigated the hypothesis that may fuel heart parasitism by activating B1R, a G protein-coupled (brady) kinin receptor whose expression is upregulated in inflamed tissues. Studies in WT and B1R mice showed that DNA levels (15 days post infection-dpi) were sharply reduced in the transgenic heart.
View Article and Find Full Text PDFIFN-γ-producing γδ T cells have been suggested to play an important role in protection against infection with Trypanosoma cruzi. However, little is known about the mechanisms leading to functional differentiation of this T cell subset in this model. In the current work, we investigated the possibility that the IL-18/MyD88 pathway is central for the generation of effector γδ T cells, playing a role for resistance against infection.
View Article and Find Full Text PDFArticle Synopsis
- TCTs from Chagas disease can trigger inflammation and microvascular leakage through the activation of innate immune cells via TLR2 and subsequent immune pathways.
- The study reveals that mast cells (MCs) play a crucial role in this inflammatory response, particularly through the activation of the kallikrein-kinin system (KKS), leading to increased bradykinin levels.
- In experiments with mice, it was found that MCs are essential for controlling the parasite load in the heart, suggesting that MC interactions with the KKS are vital for regulating inflammation during Chagas disease.