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Maternal circadian rhythm disruption affects neonatal inflammation via metabolic reprograming of myeloid cells
Zhaohai Cui1,2, Haixu Xu1, Fan Wu2,3
1Tianjin Institute of Immunology, Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), The Province and Ministry Co-sponsored Collaborative Innovation Center for Medical Epigenetics, International Joint Laboratory of Ocular Diseases, Ministry of Education, State Key Laboratory of Experimental Hematology, Department of Immunology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.
Insights
Maternal circadian rhythm disruption worsens infant inflammation. Supplementing docosahexaenoic acid (DHA) or transferring myeloid-derived suppressor cells (MDSCs) can protect against these inflammatory disorders.
Area of Science:
- Immunology
- Developmental Biology
- Metabolism
Background:
- Circadian rhythm disruption during pregnancy is linked to adverse offspring health outcomes.
- The specific impact of maternal circadian rhythms on infant immune responses and inflammation susceptibility is not well understood.
Purpose of the Study:
- To investigate the role of maternal circadian rhythms in neonatal inflammatory disorders.
- To identify mechanisms by which maternal circadian disruption affects offspring immunity.
Main Methods:
- Utilized pregnant mouse models with disrupted circadian rhythms.
- Assessed the severity of neonatal inflammatory conditions like necrotizing enterocolitis and sepsis.
- Analyzed maternal docosahexaenoic acid (DHA) levels and neonatal myeloid-derived suppressor cell (MDSC) function.
- Investigated the molecular pathways involving DHA, PPARγ, and mitochondrial oxidative phosphorylation in MDSCs.
Main Results:
- Maternal circadian disruption significantly exacerbated neonatal inflammatory disorders in offspring.
- Offspring exhibited diminished maternal DHA production and impaired immunosuppressive function of neonatal MDSCs.
- DHA was found to enhance MDSC immunosuppressive function through PPARγ-mediated mitochondrial oxidative phosphorylation.
- Transferring MDSCs or providing perinatal DHA supplementation mitigated neonatal inflammation.
Conclusions:
- Maternal circadian rhythms play a crucial role in regulating neonatal inflammation.
- Metabolic reprogramming of myeloid cells, particularly via DHA and MDSC function, is a key mechanism.
- Interventions targeting maternal circadian rhythms or DHA levels may offer protective strategies against neonatal inflammatory diseases.
Abstract:
Disruption of circadian rhythm during pregnancy produces adverse health outcomes in offspring; however, the role of maternal circadian rhythms in the immune system of infants and their susceptibility to inflammation remains poorly understood. Here we show that disruption of circadian rhythms in pregnant mice profoundly aggravates the severity of neonatal inflammatory disorders in both male and female offspring, such as necrotizing enterocolitis and sepsis. The diminished maternal production of docosahexaenoic acid (DHA) and the impaired immunosuppressive function of neonatal myeloid-derived suppressor cells (MDSCs) contribute to this phenomenon. Mechanistically, DHA enhances the immunosuppressive function of MDSCs via PPARγ-mediated mitochondrial oxidative phosphorylation. Transfer of MDSCs or perinatal supplementation of DHA relieves neonatal inflammation induced by maternal rhythm disruption. These observations collectively demonstrate a previously unrecognized role of maternal circadian rhythms in the control of neonatal inflammation via metabolic reprograming of myeloid cells.
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