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Quantification of Intracellular Growth Inside Macrophages is a Fast and Reliable Method for Assessing the Virulence of Leishmania Parasites
Published on: March 16, 2018
Modulation of Leishmania (L.) amazonensis Growth in Cultured Mouse Macrophages by Prostaglandins and Platelet
M V Lonardoni1, C L Barbieri, M Russo
1Department of Biochemistry Universidade Estadual de Maringá Paraná Brazil.
Abstract:
The role of endogenously synthesized PAF and prostaglandins on the infection of mouse macrophages by Letsbmanta (L.) amazonensis was investigated, as well as the possible correlation between the effects of these inflammatory mediators with nitric oxide production. It was found that pretreatment of macrophages with 10(-5) M of the PAF antagonists, BN-52021 or WEB-2086, increased macrophage infection by 17 and 59%, respectively. The cyclooxygenase inhibitor, indomethacin (10 mug/ml), induced a significant inhibition which was reversed by addition of PGE (10-3 M) to the culture medium. These results suggested that the infection of macrophages by leisbmanla is inhibited by PAF and enhanced by prostaglandins and that these mediators are produced by macrophages during this infection. This was confirmed by addition of these mediators to the culture medium before infection; PAF (10(-6), 10(-9) and 10(-12)M) reduced significantly the infection whereas PGE(2) (10(-5) M) induced a marked enhancement. This effect of exogenous PAF on macrophage infection was reversed by the two PAF antagonists used in this study as well as by the inhibitor of nitric oxide synthesis, L-arginine methyl ester (100 mM). Taken together the data suggest that endogenous production of PAF and PGE(2) exert opposing effects on Lesbmana-macrophage interaction and that nitric oxide may be involved in the augmented destruction of parasites induced by PAF.
Insights
Platelet-activating factor (PAF) and prostaglandins (PGE2) play opposing roles in Leishmania amazonensis macrophage infection. PAF inhibits infection, while PGE2 enhances it, with nitric oxide potentially involved in parasite destruction.
Area of Science:
- Immunology
- Parasitology
- Cell Biology
Background:
- Macrophages are key host cells for Leishmania (L.) amazonensis.
- Inflammatory mediators like platelet-activating factor (PAF) and prostaglandins (PGs) may influence parasite infection.
- The role of endogenously produced PAF and PGs in macrophage infection by L. amazonensis requires clarification.
Purpose of the Study:
- To investigate the role of endogenously synthesized PAF and prostaglandins in the infection of mouse macrophages by L. amazonensis.
- To explore the correlation between these inflammatory mediators and nitric oxide production.
- To elucidate the opposing effects of PAF and PGE2 on Leishmania-macrophage interaction.
Main Methods:
- Macrophage infection assays with L. amazonensis.
- Use of PAF antagonists (BN-52021, WEB-2086) and cyclooxygenase inhibitor (indomethacin).
- Addition of exogenous PAF and PGE2 to culture media.
- Assessment of nitric oxide synthesis inhibition using L-arginine methyl ester.
Main Results:
- PAF antagonists (BN-52021, WEB-2086) increased macrophage infection by L. amazonensis.
- Indomethacin inhibited infection, an effect reversed by PGE2.
- Exogenous PAF reduced infection, whereas PGE2 enhanced it; these effects were modulated by PAF antagonists and nitric oxide synthesis inhibition.
Conclusions:
- Endogenous PAF and PGE2 exert opposing effects on Leishmania-macrophage interaction.
- PAF inhibits, while prostaglandins enhance macrophage infection by L. amazonensis.
- Nitric oxide may be involved in PAF-induced parasite destruction within macrophages.
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