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Involvement of Extracellular ATP and Derivates in Trichomonas vaginalis Infection (pp. 187-196) $100.00
Authors:  (Amanda Piccoli Frasson, Patrícia de Brum Vieira, Tiana Tasca, Laboratório de Pesquisa em Parasitologia e Programa de Pós-Graduação em Ciências Farmacêuticas, Faculdade de Farmácia, Universidade Federal do Rio Grande do Sul, Porto Alegre, Rio Grande do Sul, Brazil)
Adenosine 5’-triphosphate (ATP) plays a crucial role in many extracellular
functions, as modulating cardiac function, blood flow, secretion, inflammation, and
immune reactions. ATP and other nucleotides can act as damage-associated molecular
patterns (DAMPs) performing a proinflammatory function in the microenvironment of
damaged cells. In the other hand, adenosine (ATP breakdown product) may revert some
of effects induced by extracellular ATP through immunosuppressive modulation. Both
ATP and adenosine play their effects by binding to specific receptors named
purinoceptors, P2 and P1, respectively. The regulation of this cell signaling is attributed
to enzymes called ectonucleotidases: the ectonucleoside triphosphate diphosphohydrolase
(E-NTPDase) family (NTPDase 1-8); the ectonucleotide pyrophosphatase/
phosphodiesterase (E-NPP) family (NPP 1-7); alkaline phosphatases, and ecto-5′-
nucleotidase (CD73). These enzymes are located at cell surfaces or found in soluble form
in the interstitial medium or in body fluids. In sequence to ecto-5’-nucleotidase activity,
adenosine deaminase (ADA) catalyses the conversion of adenosine and deoxyadenosine
to inosine and deoxyinosine, respectively. Therefore, the purinergic system constitutes an
important cellular signaling network that employs purines (especially ATP and
adenosine) and pyrimidines as signaling molecules, which can be inactivated by
ectonucleotidases, transported by cellular carriers or can also bind to purinoceptors. In
parasites the purinergic system represents an important mechanism of escape of host
immune response by ATP degradation and adenosine production, and in this manner
modulating immune response. Moreover, in spite of adenosine importance in limiting the
inflammatory response, pathogens may scavenge adenosine for growth from host cell
because these organisms lack the ability to synthesize the purine ring de novo.
Trichomonas vaginalis, a parasitic protozoan, is the etiologic agent of trichomonosis, the
most prevalent non-viral sexually transmitted disease worldwide. The investigation of
biochemical aspects of the parasite and its relationship with the host can help to clarify
some mechanisms of trichomonosis pathogenesis. NTPDase, ecto-5'-nucleotidase and
ADA activities have already been characterized in T. vaginalis trophozoites. Our group
have shown the importance of these enzymes for the parasite, since in an environment
with low concentrations of adenosine the enzymes NTPDase and ecto-5'-nucleotidase
provide the nucleoside necessary for the parasite growth. In addition, adenine nucleotides
(ATP, ADP and ATPγS) as well as ATP enzymatic hydrolysis were not decisive for nitric
oxide (NO) release by T. vaginalis-stimulated neutrophils. Unlike ATP, adenosine and
inosine decreased significantly the NO levels, revealing the immunossupressive effect of
adenosine – promoted by A2A activation - and the importance of ecto-5’-nucleotidase
activity of T. vaginalis during the establishment of trichomonosis. Considering the high
concentration of extracellular ATP at the infection site, the purinergic system represents a
primordial form of chemical intercellular signaling where the ectonucleotidases of the
parasite play an important role. The enzymes hydrolyze ATP producing adenosine which
will be uptaked and employed for the parasite growth and moreover, the antiinflammatory
effects of the nucleoside can contribute to the effectiveness of infection. In
this context, the enzymes may be considered pathogenic markers in the identification of
T. vaginalis isolates as well as future possible adjuncts on diagnosis and interesting
targets of new alternatives for the treatment of trichomonosis. 

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Involvement of Extracellular ATP and Derivates in <i>Trichomonas vaginalis</i> Infection (pp. 187-196)