Crosstalk between purinergic receptors and lipid mediators in leishmaniasis.
Leishmaniasis is a neglected tropical disease affecting millions of people around the world caused by organisms of the genus Leishmania. Parasite escape mechanisms of the immune system confer the possibility of resistance and dissemination of the disease. A group of molecules that has become a target for Leishmania survival strategies are lipid mediators. Among them, leukotriene B4 (LTB4) has been described as a pro-inflammatory molecule capable of activating cells of the immune system to combat Leishmania. In an opposite way, prostaglandin E2 (PGE2) is a lipid mediator described as a deactivator of macrophages and neutrophils. The balance of these two molecules can be generated by extracellular nucleotides, such as adenosine 5'-triphosphate (ATP) and adenosine (Ado), which activate the purinergic receptors system. Herein, we discuss the role of extracellular nucleotides and the resulting balance of LTB4 and PGE2 in Leishmania fate, survival or death.
Laboratory of Immunophysiology, Biophysics Institute Carlos Chagas Filho, Federal University of Rio de Janeiro, Rio de Janeiro, RJ, 21941-902, Brazil.|Laboratory of Inflammation, Biophysics Institute Carlos Chagas Filho, Federal University of Rio de Janeiro, Rio de Janeiro, RJ, 21941-902, Brazil.|National Institute of Translational Research in Health and Environment in the Amazon Region, Biophysics Institute Carlos Chagas Filho, Federal University of Rio de Janeiro, Rio de Janeiro, RJ, 21941-902, Brazil.
Mariana M
MM
Chaves
Laboratory of Inflammation, Biophysics Institute Carlos Chagas Filho, Federal University of Rio de Janeiro, Rio de Janeiro, RJ, 21941-902, Brazil.|National Institute of Translational Research in Health and Environment in the Amazon Region, Biophysics Institute Carlos Chagas Filho, Federal University of Rio de Janeiro, Rio de Janeiro, RJ, 21941-902, Brazil.
Cláudio
C
Canetti
Laboratory of Immunophysiology, Biophysics Institute Carlos Chagas Filho, Federal University of Rio de Janeiro, Rio de Janeiro, RJ, 21941-902, Brazil. rcsilva@biof.ufrj.br.|National Institute of Translational Research in Health and Environment in the Amazon Region, Biophysics Institute Carlos Chagas Filho, Federal University of Rio de Janeiro, Rio de Janeiro, RJ, 21941-902, Brazil. rcsilva@biof.ufrj.br.
Robson
R
Coutinho-Silva
D000241:Adenosine; D000255:Adenosine Triphosphate; D000818:Animals; D015232:Dinoprostone / Q000378:metabolism*; D006801:Humans; D057131:Immune Evasion; D007891:Leishmania / Q000276:immunology / Q000502:physiology*; D007896:Leishmaniasis / Q000276:immunology / Q000378:metabolism* / Q000469:parasitology*; D007975:Leukotriene B4 / Q000378:metabolism*; D008264:Macrophages / Q000378:metabolism; D051379:Mice; D009504:Neutrophils / Q000378:metabolism; D020239:Receptor Cross-Talk; D011983:Receptors, Purinergic / Q000378:metabolism*
D011983:Receptors, Purinergic; D007975:Leukotriene B4; D000255:Adenosine Triphosphate; D000241:Adenosine; D015232:Dinoprostone