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Prostaglandin E2/Leukotriene B 4 balance induced by Lutzomyia longipalpis saliva favors Leishmania infantum infection

BACKGROUND: Eicosanoids and sand fly saliva have a critical role in the Leishmania infection. Here, we evaluated the effect of Lutzomyia longipalpis salivary gland sonicate (SGS) on neutrophil and monocyte recruitment and activation of eicosanoid production in a murine model of inflammation. METHODS...

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Bibliographic Details
Published in:Parasites & vectors 2014, Vol.7 (1)
Main Authors: Araújo-Santos, Théo, Prates, Deboraci Brito, França-Costa, Jaqueline, Luz, Nívea F, Andrade, Bruno B, Miranda, José Carlos, Brodskyn, Claudia I, Barral, Aldina, Bozza, Patrícia T, Borges, Valéria Matos
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Language:English
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Summary:BACKGROUND: Eicosanoids and sand fly saliva have a critical role in the Leishmania infection. Here, we evaluated the effect of Lutzomyia longipalpis salivary gland sonicate (SGS) on neutrophil and monocyte recruitment and activation of eicosanoid production in a murine model of inflammation. METHODS: C57BL/6 mice were inoculated intraperitonealy with Lutzomyia longipalpis SGS or Leishmania infantum or both, followed by analyses of cell recruitment, parasite load and eicosanoid production. RESULTS: Intraperitoneal injection of Lutzomyia longipalpis SGS together with Leishmania infantum induced an early increased parasite viability in monocytes and neutrophils. L. longipalpis SGS increased prostaglandin E₂(PGE₂), but reduced leukotriene B₄(LTB₄) production ex vivo in peritoneal leukocytes. In addition, the pharmacological inhibition of cyclooxygenase 2 (COX-2) with NS-398 decreased parasite viability inside macrophages during Leishmania infection in the presence of L. longipalpis SGS arguing that PGE₂production is associated with diminished parasite killing. CONCLUSIONS: These findings indicate that L. longipalpis SGS is a critical factor driving immune evasion of Leishmania through modulation of PGE₂/LTB₄axis, which may represent an important mechanism on establishment of the infection.
ISSN:1756-3305
1756-3305