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DHA Suppresses Primary Macrophage Inflammatory Responses via Notch 1/ Jagged 1 Signaling

Mehboob Ali1, Kathryn Heyob1, Lynette K Rogers1,2

  • 1Center for Perinatal Research, The Research Institute at Nationwide Children's Hospital, Columbus, Ohio, USA.

Scientific Reports
|March 5, 2016
PubMed

Insights

Maternal docosahexaenoic acid (DHA) supplementation reduced persistent lung macrophages and improved offspring lung development. DHA also attenuated inflammatory markers like Notch 1/Jagged 1 and leukotriene B4, protecting epithelial cells.

Area of Science:

  • Pulmonary immunology
  • Developmental biology
  • Nutritional science

Background:

  • Persistent macrophages in offspring lungs are linked to maternal LPS and neonatal hyperoxia exposure.
  • Docosahexaenoic acid (DHA) supplementation during pregnancy may mitigate these adverse effects on lung development.

Purpose of the Study:

  • To investigate the role of macrophages in lung pathologies induced by maternal LPS and neonatal hyperoxia.
  • To determine the mechanisms by which maternal DHA supplementation exerts protective effects on lung development.

Main Methods:

  • Primary mouse macrophages were isolated and exposed to hyperoxia and LPS in vitro.
  • In vivo studies involved maternal DHA supplementation in mice exposed to LPS and hyperoxia.
  • Co-culture experiments assessed macrophage-epithelial cell interactions and inflammatory mediator release.

Main Results:

  • In vivo DHA supplementation significantly reduced Notch 1 and Jagged 1 protein levels in lungs.
  • In vitro DHA supplementation suppressed leukotriene B4 release and protected epithelial cells in co-culture.
  • Maternal DHA supplementation prevented macrophage accumulation and improved lung development in offspring.

Conclusions:

  • Long-term in vivo DHA supplementation reduces Notch 1/Jagged 1 expression and improves lung development.
  • In vitro DHA supplementation protects epithelial cells by suppressing inflammatory mediator release, suggesting a dual protective mechanism.

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