Cyclic AMP decreases the production of NO and CCL2 by macrophages stimulated with Trypanosoma cruzi GPI-mucins.
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2009
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Glycosylphosphatidylinositol-anchored mucinlike
glycoproteins (tGPI-mucin) present on the surface of
the cellular membrane of Trypanosoma cruzi forms activate
toll-like receptors 2 (TLR2) on the surface of immune cells
and induce the release of several mediators of inflammation
which may be relevant in the context of Chagas disease.
Here, we evaluated the ability of tGPI-mucins to activate
murine peritoneal macrophages to induce nitric oxide (NO)
and monocyte chemoattractant protein-1 (MCP-1/CCL2).
We also investigated the ability of compounds which
increase or mimic cyclic adenosine monophosphate
(AMP) to modulate the production of NO and CCL2. Our
data show that elevation of intracellular levels of cyclic
AMP prevents the release of NO and CCL2 induced by
tGPI-mucins in macrophages. Overall, the release of CCL2
was decreased to a greater extent and at lower concentrations
of cyclic AMP-modifying agents than the production
of NO. It is suggested that the elevation of cyclic AMP
during T. cruzi infection may modify the release of proinflammatory
mediators and alter significantly the course of
T. cruzi infection.
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TALVANI, A. et al. Cyclic AMP decreases the production of NO and CCL2 by macrophages stimulated with Trypanosoma cruzi GPI-mucins. Parasitology Research, v. 104, p. 1141-1148, 2009. Disponível em: <http://link.springer.com/article/10.1007%2Fs00436-008-1300-1>. Acesso em: 19 fev. 2017.