Distinctive histopathology and modulation of cytokine production during oral and intraperitoneal Trypanosoma cruzi Y strain infection.

Acute Chagas disease outbreaks are related to the consumption of food or drink contaminated by triatomine feces, thus making oral infection an important route of transmission. Both vector-borne and oral infections trigger important cardiac manifestations in the host that are related to a dysregulated immune response. The aims of this work were to evaluate possible alterations of lymphocyte CD4+/CD8+ sub-populations, Th1 and Th2 cytokines, nitrite concentrations and cardiac histopathology.

Prior and concomitant dehydroepiandrosterone treatment affects immunologic response of cultured macrophages infected with Trypanosoma cruzi in vitro?

DHEA, a steroid hormone synthesized from cholesterol by cells of the adrenal cortex, plays an essential role in enhancing the host's resistance to different experimental infections. Receptors for this hormone can be found in distinct immune cells (especially macrophages) that are known to be the first line defense against Trypanosoma cruzi infection. These cells operate through an indirect pathway releasing nitric oxide (NO) and cytokines such TNF-α and IL-12 which in turn trigger an enhancement of natural killer cells and lymphocytes which finally secrete pro and anti-inflammatory cytokines.