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Estudio2019Solo mecanismos

Docosahexaenoic acid enhances M2 macrophage polarization via the p38 signaling pathway and autophagy

Kawano A, Ariyoshi W, Yoshioka Y, Hikiji H, Nishihara T, Okinaga T

Journal of cellular biochemistry · 76 citas

Etiquetas de revisión

Solo mecanismos

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Cómo se estudió

Diseño
Estudio in vitro o de mecanismos (clasificado por nuestro filtro de IA)
Estudiado en
Células o muestras de laboratorio
Resultado principal
Solo mecanismos

Quién lo pagó

Financiación
Financiación independiente
Gobierno
Japan Society for the Promotion of Science
Gobierno
Scientific Research from the Japan Society for the Promotion of Science
Subvenciones
Japan Society for the Promotion of Science (18K09556); Japan Society for the Promotion of Science (19K10340)

Según 2 financiadores declarados.

Publicación

Publicado
2019-03-01 · J Cell Biochem · vol. 120 · número 8 · págs. 12604–12617
Editorial
Wiley
Citado
92 citas · más que el 94% de estudios similares · 3.6× el promedio de su campo
Impacto
Entre el 10 % más citado de su campo
Referencias
44 trabajos
Acceso
De pago
Áreas de investigación
Immune cells in cancer · IL-33, ST2, and ILC Pathways · Inflammasome and immune disorders
Palabras clave
Cell biology, Proinflammatory cytokine, Macrophage polarization, p38 mitogen-activated protein kinases, Docosahexaenoic acid, Signal transduction, Autophagy, U937 cell, MAPK/ERK pathway, M2 Macrophage, Biology, CD14, Inflammation, Chemistry, Macrophage, Biochemistry, Immune system, Immunology, Polyunsaturated fatty acid, Fatty acid
MeSH
u937 cells, macrophages, humans, inflammation, docosahexaenoic acids, anti-inflammatory agents, interleukin-4, map kinase signaling system, autophagy, thp-1 cells, kruppel-like factor 4

6 autores

  • Aki Kawano🇯🇵Kyushu Dental University
  • Wataru Ariyoshi🇯🇵Kyushu Dental University
  • Yoshie Yoshioka🇯🇵Kyushu Dental University
  • Hisako Hikiji🇯🇵Kyushu Dental University
  • Tatsuji Nishihara🇯🇵Kyushu Dental University
  • Toshinori Okinaga🇯🇵 · autor de correspondenciaOsaka Dental University

Resumen

El texto original del estudio, en el idioma en que se publicó.

Macrophages, critical modulators of the immune response, polarize into various phenotypes, including M1 and M2. M1 macrophages are typically activated by lipopolysaccharide and produce proinflammatory cytokines. Conversely, M2 macrophages are activated by stimulation with interleukin 4 (IL)-4 and promote tissue remodeling and anti-inflammatory reactions. Recently, polyunsaturated fatty acids (PUFAs) have been shown to play important roles in the regulation of inflammation. Docosahexaenoic acid (DHA), a PUFA, has anti-inflammatory effects on chronic inflammatory disease, but its role in macrophage polarization remains unclear. In this study, we clarified the effects of DHA on macrophage polarization using U937 cells. Treatment with DHA resulted in upregulation of M2 macrophage markers and increased secretion of anti-inflammatory cytokines by U937 cells. IL-4, but not DHA, triggered phosphorylation of signal transducer and activator of transcription 6 (STAT6). DHA enhanced the expression of krüppel-like factor-4 (KLF4), a transcription factor involved in the regulation of macrophage polarization and increased the phosphorylation of p38 mitogen-activated protein kinase (MAPK). A selective inhibitor of p38 MAPK downregulated the expression of CD206 in DHA-treated U937 cells. Moreover, inhibitors of autophagy suppressed the phosphorylation of p38 MAPK and the expression of CD206 in DHA-treated U937 cells. Expression of microtubule-associated protein light chain 3-II, which is involved in autophagosome formation, was enhanced in DHA-treated U937 cells. Taken together, these results indicated that DHA enhanced the expression of M2 macrophage markers through the p38 MAPK signaling pathway and autophagy, suggesting that DHA regulates M2 macrophage polarization and plays an important role in innate immunity.

Resumen vía Europe PMC. Los derechos de autor siguen siendo de los autores o la editorial.

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