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Resolvin D1 drives establishment of Leishmania amazonensis infection

Previous studies have indicated that the balance between different eicosanoids reflect the intensity of the inflammatory profile in patients with tegumentary leishmaniasis. More recently, pro-resolution lipid mediators have been shown to play critical roles in dampening pathological inflammatory pro...

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Autores principales: Malta-Santos, Hayna, Andrade, Bruno B., Zanette, Dalila L., Costa, Jackson M., Bozza, Patrícia T., Bandeira-Melo, Christianne, Barral, Aldina, França-Costa, Jaqueline, Borges, Valéria M.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group 2017
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Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5385529/
https://www.ncbi.nlm.nih.gov/pubmed/28393908
http://dx.doi.org/10.1038/srep46363
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author Malta-Santos, Hayna
Andrade, Bruno B.
Zanette, Dalila L.
Costa, Jackson M.
Bozza, Patrícia T.
Bandeira-Melo, Christianne
Barral, Aldina
França-Costa, Jaqueline
Borges, Valéria M.
author_facet Malta-Santos, Hayna
Andrade, Bruno B.
Zanette, Dalila L.
Costa, Jackson M.
Bozza, Patrícia T.
Bandeira-Melo, Christianne
Barral, Aldina
França-Costa, Jaqueline
Borges, Valéria M.
author_sort Malta-Santos, Hayna
collection PubMed
description Previous studies have indicated that the balance between different eicosanoids reflect the intensity of the inflammatory profile in patients with tegumentary leishmaniasis. More recently, pro-resolution lipid mediators have been shown to play critical roles in dampening pathological inflammatory processes to reestablish homeostasis in a diverse range of experimental settings. Among these lipid mediator, resolvins from D series have been described as potent anti-inflammatory and immunomodulatory mediators, and its activities include inhibition of leukocyte chemotaxis and blockage production of proinflammatory cytokines, while increasing the expression of regulatory mediators. Whether resolvins play significant roles in establishment and persistence of Leishmania infection is currently unknown. We addressed this question in the current study by assessing circulating levels of D-series resolvins in tegumentary leishmaniasis patients presenting with localized or diffuse disease. We found heightened expression of resolvin D1 in diffuse cutaneous leishmaniasis which was correlated with expression profile of biomarkers associated with disease pathogenesis. Additional in vitro experiments using primary human macrophages indicated that resolvin D1 may promote intracellular Leishmania amazonensis replication through a mechanism associated with induction of heme oxygenase-1. These results suggest that targeting resolvin D1 could serve as potential strategy for host directed therapy in diffuse cutaneous leishmaniasis.
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spelling pubmed-53855292017-04-12 Resolvin D1 drives establishment of Leishmania amazonensis infection Malta-Santos, Hayna Andrade, Bruno B. Zanette, Dalila L. Costa, Jackson M. Bozza, Patrícia T. Bandeira-Melo, Christianne Barral, Aldina França-Costa, Jaqueline Borges, Valéria M. Sci Rep Article Previous studies have indicated that the balance between different eicosanoids reflect the intensity of the inflammatory profile in patients with tegumentary leishmaniasis. More recently, pro-resolution lipid mediators have been shown to play critical roles in dampening pathological inflammatory processes to reestablish homeostasis in a diverse range of experimental settings. Among these lipid mediator, resolvins from D series have been described as potent anti-inflammatory and immunomodulatory mediators, and its activities include inhibition of leukocyte chemotaxis and blockage production of proinflammatory cytokines, while increasing the expression of regulatory mediators. Whether resolvins play significant roles in establishment and persistence of Leishmania infection is currently unknown. We addressed this question in the current study by assessing circulating levels of D-series resolvins in tegumentary leishmaniasis patients presenting with localized or diffuse disease. We found heightened expression of resolvin D1 in diffuse cutaneous leishmaniasis which was correlated with expression profile of biomarkers associated with disease pathogenesis. Additional in vitro experiments using primary human macrophages indicated that resolvin D1 may promote intracellular Leishmania amazonensis replication through a mechanism associated with induction of heme oxygenase-1. These results suggest that targeting resolvin D1 could serve as potential strategy for host directed therapy in diffuse cutaneous leishmaniasis. Nature Publishing Group 2017-04-10 /pmc/articles/PMC5385529/ /pubmed/28393908 http://dx.doi.org/10.1038/srep46363 Text en Copyright © 2017, The Author(s) http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/
spellingShingle Article
Malta-Santos, Hayna
Andrade, Bruno B.
Zanette, Dalila L.
Costa, Jackson M.
Bozza, Patrícia T.
Bandeira-Melo, Christianne
Barral, Aldina
França-Costa, Jaqueline
Borges, Valéria M.
Resolvin D1 drives establishment of Leishmania amazonensis infection
title Resolvin D1 drives establishment of Leishmania amazonensis infection
title_full Resolvin D1 drives establishment of Leishmania amazonensis infection
title_fullStr Resolvin D1 drives establishment of Leishmania amazonensis infection
title_full_unstemmed Resolvin D1 drives establishment of Leishmania amazonensis infection
title_short Resolvin D1 drives establishment of Leishmania amazonensis infection
title_sort resolvin d1 drives establishment of leishmania amazonensis infection
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5385529/
https://www.ncbi.nlm.nih.gov/pubmed/28393908
http://dx.doi.org/10.1038/srep46363
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