High-Density lipoproteins decrease proinflammatory activity and modulate the innate immune response
Atherosclerosis, a chronic inflammatory disease of the arterial wall, is the leading cause of cardiac disorders and stroke. The onset and progression of these diseases are linked with the inflammatory response, especially NLRP3 inflammasome activation, inducing the production of proinflammatory cyto...
- Autores:
-
Taborda, Natalia Andrea
Blanquiceth, Yurany
Urcuqui Inchima, Silvio
Latz, Eicke
Hernández López, Juan Carlos
- Tipo de recurso:
- Article of journal
- Fecha de publicación:
- 2019
- Institución:
- Universidad Cooperativa de Colombia
- Repositorio:
- Repositorio UCC
- Idioma:
- OAI Identifier:
- oai:repository.ucc.edu.co:20.500.12494/28300
- Acceso en línea:
- https://hdl.handle.net/20.500.12494/28300
- Palabra clave:
- Atherosclerosis
- Rights
- openAccess
- License
- Atribución
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dc.title.spa.fl_str_mv |
High-Density lipoproteins decrease proinflammatory activity and modulate the innate immune response |
title |
High-Density lipoproteins decrease proinflammatory activity and modulate the innate immune response |
spellingShingle |
High-Density lipoproteins decrease proinflammatory activity and modulate the innate immune response Atherosclerosis |
title_short |
High-Density lipoproteins decrease proinflammatory activity and modulate the innate immune response |
title_full |
High-Density lipoproteins decrease proinflammatory activity and modulate the innate immune response |
title_fullStr |
High-Density lipoproteins decrease proinflammatory activity and modulate the innate immune response |
title_full_unstemmed |
High-Density lipoproteins decrease proinflammatory activity and modulate the innate immune response |
title_sort |
High-Density lipoproteins decrease proinflammatory activity and modulate the innate immune response |
dc.creator.fl_str_mv |
Taborda, Natalia Andrea Blanquiceth, Yurany Urcuqui Inchima, Silvio Latz, Eicke Hernández López, Juan Carlos |
dc.contributor.author.none.fl_str_mv |
Taborda, Natalia Andrea Blanquiceth, Yurany Urcuqui Inchima, Silvio Latz, Eicke Hernández López, Juan Carlos |
dc.subject.spa.fl_str_mv |
Atherosclerosis |
topic |
Atherosclerosis |
description |
Atherosclerosis, a chronic inflammatory disease of the arterial wall, is the leading cause of cardiac disorders and stroke. The onset and progression of these diseases are linked with the inflammatory response, especially NLRP3 inflammasome activation, inducing the production of proinflammatory cytokines, such as interleukin 1b (IL-1b). Because high-density lipoproteins (HDLs) have shown significant antiatherogenic and antiinflammatory properties, we evaluated their immunomodulatory activity in response to cholesterol crystals and other innate immune activators. Human primary monocyte-derived macrophages, THP-1 cells, and murine macrophages were stimulated to activate NLRP3 inflammasome and other pattern recognition receptors, in the presence or absence of HDL. Then, HDL immunomodulatory effects were evaluated through IL-1b and IL-6 production by enzyme-linked immunosorbent assay. Furthermore, in vivo HDL antiinflammatory effects were evaluated in a murine model of peritoneal inflammatory infiltration. HDLs have an immunomodulatory effect on different cellular models, including peripheral blood mononuclear cells, THP-1 cells, and murine macrophages, by affecting the activity of innate immunity sensors, such as Toll-like receptors (TLRs), dectin-1, and inflammasomes. HDL reduces the proinflammatory role of cholesterol crystals, nigericin, and other NLRP3 and AIM2 inflammasome agonists, and several TLR agonists, leading to a decreased production of IL-1b and IL-6. The results suggest that HDLs are highly important in the regulation of the innate immune response and may have a beneficial role in controlling diseases associated with the inflammatory response. |
publishDate |
2019 |
dc.date.issued.none.fl_str_mv |
2019-12-01 |
dc.date.accessioned.none.fl_str_mv |
2020-11-27T00:59:20Z |
dc.date.available.none.fl_str_mv |
2020-11-27T00:59:20Z |
dc.type.none.fl_str_mv |
Artículo |
dc.type.coar.fl_str_mv |
http://purl.org/coar/resource_type/c_2df8fbb1 |
dc.type.coar.none.fl_str_mv |
http://purl.org/coar/resource_type/c_6501 |
dc.type.coarversion.none.fl_str_mv |
http://purl.org/coar/version/c_970fb48d4fbd8a85 |
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info:eu-repo/semantics/article |
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info:eu-repo/semantics/publishedVersion |
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http://purl.org/coar/resource_type/c_6501 |
status_str |
publishedVersion |
dc.identifier.uri.spa.fl_str_mv |
10.1089/jir.2019.0029 |
dc.identifier.uri.none.fl_str_mv |
https://hdl.handle.net/20.500.12494/28300 |
dc.identifier.bibliographicCitation.spa.fl_str_mv |
Taborda, N. A., Blanquiceth, Y., Urcuqui-Inchima, S., Latz, E., y Hernandez, J. C. (2019). High-Density Lipoproteins Decrease Proinflammatory Activity and Modulate the Innate Immune Response. Journal of Interferon & Cytokine Research, 39 (12), 760-770. Recuperado de https://www.liebertpub.com/doi/abs/10.1089/jir.2019.0029 |
identifier_str_mv |
10.1089/jir.2019.0029 Taborda, N. A., Blanquiceth, Y., Urcuqui-Inchima, S., Latz, E., y Hernandez, J. C. (2019). High-Density Lipoproteins Decrease Proinflammatory Activity and Modulate the Innate Immune Response. Journal of Interferon & Cytokine Research, 39 (12), 760-770. Recuperado de https://www.liebertpub.com/doi/abs/10.1089/jir.2019.0029 |
url |
https://hdl.handle.net/20.500.12494/28300 |
dc.relation.isversionof.spa.fl_str_mv |
https://www.liebertpub.com/doi/abs/10.1089/jir.2019.0029 |
dc.relation.ispartofjournal.spa.fl_str_mv |
Journal of Interferon & Cytokine Research |
dc.relation.references.spa.fl_str_mv |
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Taborda, Natalia AndreaBlanquiceth, YuranyUrcuqui Inchima, SilvioLatz, EickeHernández López, Juan Carlos39 (12)2020-11-27T00:59:20Z2020-11-27T00:59:20Z2019-12-0110.1089/jir.2019.0029https://hdl.handle.net/20.500.12494/28300Taborda, N. A., Blanquiceth, Y., Urcuqui-Inchima, S., Latz, E., y Hernandez, J. C. (2019). High-Density Lipoproteins Decrease Proinflammatory Activity and Modulate the Innate Immune Response. Journal of Interferon & Cytokine Research, 39 (12), 760-770. Recuperado de https://www.liebertpub.com/doi/abs/10.1089/jir.2019.0029Atherosclerosis, a chronic inflammatory disease of the arterial wall, is the leading cause of cardiac disorders and stroke. The onset and progression of these diseases are linked with the inflammatory response, especially NLRP3 inflammasome activation, inducing the production of proinflammatory cytokines, such as interleukin 1b (IL-1b). Because high-density lipoproteins (HDLs) have shown significant antiatherogenic and antiinflammatory properties, we evaluated their immunomodulatory activity in response to cholesterol crystals and other innate immune activators. Human primary monocyte-derived macrophages, THP-1 cells, and murine macrophages were stimulated to activate NLRP3 inflammasome and other pattern recognition receptors, in the presence or absence of HDL. Then, HDL immunomodulatory effects were evaluated through IL-1b and IL-6 production by enzyme-linked immunosorbent assay. Furthermore, in vivo HDL antiinflammatory effects were evaluated in a murine model of peritoneal inflammatory infiltration. HDLs have an immunomodulatory effect on different cellular models, including peripheral blood mononuclear cells, THP-1 cells, and murine macrophages, by affecting the activity of innate immunity sensors, such as Toll-like receptors (TLRs), dectin-1, and inflammasomes. HDL reduces the proinflammatory role of cholesterol crystals, nigericin, and other NLRP3 and AIM2 inflammasome agonists, and several TLR agonists, leading to a decreased production of IL-1b and IL-6. The results suggest that HDLs are highly important in the regulation of the innate immune response and may have a beneficial role in controlling diseases associated with the inflammatory response.Atherosclerosis, a chronic inflammatory disease of the arterial wall, is the leading cause of cardiac disorders and stroke. The onset and progression of these diseases are linked with the inflammatory response, especially NLRP3 inflammasome activation, inducing the production of proinflammatory cytokines, such as interleukin 1b (IL-1b). Because high-density lipoproteins (HDLs) have shown significant antiatherogenic and antiinflammatory properties, we evaluated their immunomodulatory activity in response to cholesterol crystals and other innate immune activators. Human primary monocyte-derived macrophages, THP-1 cells, and murine macrophages were stimulated to activate NLRP3 inflammasome and other pattern recognition receptors, in the presence or absence of HDL. Then, HDL immunomodulatory effects were evaluated through IL-1b and IL-6 production by enzyme-linked immunosorbent assay. Furthermore, in vivo HDL antiinflammatory effects were evaluated in a murine model of peritoneal inflammatory infiltration. HDLs have an immunomodulatory effect on different cellular models, including peripheral blood mononuclear cells, THP-1 cells, and murine macrophages, by affecting the activity of innate immunity sensors, such as Toll-like receptors (TLRs), dectin-1, and inflammasomes. HDL reduces the proinflammatory role of cholesterol crystals, nigericin, and other NLRP3 and AIM2 inflammasome agonists, and several TLR agonists, leading to a decreased production of IL-1b and IL-6. The results suggest that HDLs are highly important in the regulation of the innate immune response and may have a beneficial role in controlling diseases associated with the inflammatory response.https://scienti.colciencias.gov.co/cvlac/visualizador/generarCurriculoCv.do?cod_rh=0000283088http://orcid.org/0000-0002-9200-5698https://scienti.colciencias.gov.co/gruplac/jsp/visualiza/visualizagr.jsp?nro=00000000011355juanc.hernandezl@campusucc.edu.cohttps://scholar.google.com/citations?user=fo79p5QAAAAJ&hl=es760-770Mary Ann Liebert, Inc., publishersUniversidad Cooperativa de Colombia, Facultad de Ciencias de la Salud, Programa de Medicina, Medellín y Envigado, Colombia, 00000MedicinaMedellínhttps://www.liebertpub.com/doi/abs/10.1089/jir.2019.0029Journal of Interferon & Cytokine ResearchBarrientos-Arenas E, Henao-García V, Giraldo DM, Cardona MM, Urcuqui Inchima S, Castaño JC, Hernández JC. 2018. 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