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Breast Milk-Derived Extracellular Vesicles Enriched in Exosomes From Mothers With Type 1 Diabetes Contain Aberrant Levels of microRNAs

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review


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  • Aashiq H Mirza
  • Simranjeet Kaur
  • Lotte B Nielsen
  • Joachim Størling
  • Reza Yarani
  • Martin Roursgaard
  • Elisabeth R Mathiesen
  • Peter Damm
  • Jens Svare
  • Henrik B Mortensen
  • Flemming Pociot
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The breast milk plays a crucial role in shaping the initial intestinal microbiota and mucosal immunity of the infant. Interestingly, breastfeeding has proven to be protective against the early onset of immune-mediated diseases including type 1 diabetes. Studies have shown that exosomes from human breast milk are enriched in immune-modulating miRNAs suggesting that exosomal miRNAs (exomiRs) transferred to the infant could play a critical role in the development of the infant's immune system. We extracted exomiRs from breast milk of 52 lactating mothers (26 mothers with type 1 diabetes and 26 healthy mothers), to identify any differences in the exomiR content between the two groups. Small RNA-sequencing was performed to identify known and novel miRNAs in both groups. A total of 631 exomiRs were detected by small RNA sequencing including immune-related miRNAs such as hsa-let-7c, hsa-miR-21, hsa-miR-34a, hsa-miR-146b, and hsa-miR-200b. In addition, ~200 novel miRNAs were identified in both type 1 diabetes and control samples. Among the known miRNAs, nine exomiR's were found differentially expressed in mothers with type 1 diabetes compared to healthy mothers. The highly up-regulated miRNAs, hsa-miR-4497, and hsa-miR-3178, increased lipopolysaccharide-induced expression and secretion of tumor necrosis factor α (TNFα) in human monocytes. The up-regulated miRNA target genes were significantly enriched for longevity-regulating pathways and FoxO signaling. Our findings suggest a role of breast milk-derived exomiRs in modulating the infant's immune system.

TidsskriftFrontiers in Immunology
Sider (fra-til)1-10
Antal sider10
StatusUdgivet - okt. 2019

Bibliografisk note

Copyright © 2019 Mirza, Kaur, Nielsen, Størling, Yarani, Roursgaard, Mathiesen, Damm, Svare, Mortensen and Pociot.

ID: 58351358