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Eosinophils increase macrophage ability to control intracellular Leishmania amazonensis infection via PGD2 paracrine activity in vitro
•Eosinophils enhance macrophage ability to control intracellular L. amazonensis infection in vitro.•Eosinophil-driven mechanism depends on a paracrine activity mediated by soluble factor(s).•Eosinophil-secreted PGD2 mediates enhanced macrophage ability to manage L. amazonensis infection.•Macrophage...
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Published in: | Cellular immunology 2021-05, Vol.363, p.104316-104316, Article 104316 |
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Main Authors: | , , , , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | •Eosinophils enhance macrophage ability to control intracellular L. amazonensis infection in vitro.•Eosinophil-driven mechanism depends on a paracrine activity mediated by soluble factor(s).•Eosinophil-secreted PGD2 mediates enhanced macrophage ability to manage L. amazonensis infection.•Macrophage DP2 receptors mediate the effect of eosinophil-derived PGD2.•Eosinophil/PGD2 may be adjuvant therapeutic option in L. amazonensis-driven diseases.
Clinical and experimental studies have described eosinophil infiltration in Leishmania amazonensis infection sites, positioning eosinophils strategically adjacent to the protozoan-infected macrophages in cutaneous leishmaniasis. Here, by co-culturing mouse eosinophils with L. amazonensis-infected macrophages, we studied the impact of eosinophils on macrophage ability to regulate intracellular L. amazonensis infection. Eosinophils prevented the increase in amastigote numbers within macrophages by a mechanism dependent on a paracrine activity mediated by eosinophil-derived prostaglandin (PG) D2 acting on DP2 receptors. Exogenous PGD2 mimicked eosinophil-mediated effect on managing L. amazonensis intracellular infection by macrophages and therefore may function as a complementary tool for therapeutic intervention in L. amazonensis-driven cutaneous leishmaniasis. |
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ISSN: | 0008-8749 1090-2163 |
DOI: | 10.1016/j.cellimm.2021.104316 |