ATPe Dynamics in Protozoan Parasites. Adapt or Perish

Abstract

In most animals, transient increases of extracellular ATP (ATPe) are used for physiological signaling or as a danger signal in pathological conditions. ATPe dynamics are controlled by ATP release from viable cells and cell lysis, ATPe degradation and interconversion by ecto-nucleotidases, and interaction of ATPe and byproducts with cell surface purinergic receptors and purine salvage mechanisms. Infection by protozoan parasites may alter at least one of the mechanisms controlling ATPe concentration. Protozoan parasites display their own set of proteins directly altering ATPe dynamics, or control the activity of host proteins. Parasite dependent activation of ATPe conduits of the host may promote infection and systemic responses that are beneficial or detrimental to the parasite. For instance, activation of organic solute permeability at the host membrane can support the elevated metabolism of the parasite. On the other hand ecto-nucleotidases of protozoan parasites, by promoting ATPe degradation and purine/pyrimidine salvage, may be involved in parasite growth, infectivity, and virulence. In this review, we will describe the complex dynamics of ATPe regulation in the context of protozoan parasite–host interactions. Particular focus will be given to features of parasite membrane proteins strongly controlling ATPe dynamics. This includes evolutionary, genetic and cellular mechanisms, as well as structural-functional relationships.

Involvement of ectonucleotidases and purinergic receptor expression during acute Chagas disease in the cortex of mice treated with resveratrol and benznidazole

“…These results suggest a suitable immunosuppressive effect of RSV during acute T. cruzi infection [47]. Therefore, ADA is related to vital functions of the parasites such as Trypanosoma evansi [48] and Plasmodium falciparum [49], since this enzyme is responsible for degrading adenosine in inosine, which is later used in the purine rescue pathway of these parasites [50]. Thus, our data suggest that treatments with BNZ or RSV modulate ADA activity, reduce ADO levels and convert inosine by E-ADA, and suppress immune responses.…”