IL-1β directly inhibits milk lipid production in lactating mammary epithelial cells concurrently with enlargement of cytoplasmic lipid droplets

Kota Matsunaga, Yusaku Tsugami, Aogu Kumai, Takahiro Suzuki, Takanori Nishimura, Ken Kobayashi

Research output: Contribution to journalArticlepeer-review

5 Citations (Scopus)

Abstract

Mammary epithelial cells (MECs) in lactating mammary glands produce milk lipid, which provides a large percentage of calories and bioactive lipids for appropriate infant growth. However, secreted milk lipid is often reduced concurrently with increases in IL-1β IL-6, and TNF-α in mammary glands with mastitis. In this study, we investigated whether those cytokines directly influenced lipid production and secretion. A lactating MEC culture model with high lipid production ability was prepared by culture with oleic acid. TNF-α IL-1β and IL-6 differentially affected lipid production and secretion in lactating MECs. In particular, IL-1β treatment significantly reduced amounts of secreted triglycerides by 97% compared with the control concurrently with enlargement of cytoplasmic lipid droplets in MECs. IL-1β also decreased mRNA expression of Fabp3 and Srebp1 and the amount of aquaporin 3, GLUT-1 and adipophilin in the milk lipid production pathway. Furthermore, IL-1β inactivated STAT5 and glucocorticoid signaling to induce milk production in MECs, whereas STAT3 and NFκB signaling was activated. IL-1β induced mRNA expression of IL-6 and TNF-α in MECs. Therefore, we suggest that IL-1β is a key inhibitor of lipid production and secretion in lactating MECs.

Original languageEnglish
Pages (from-to)365-372
Number of pages8
JournalExperimental Cell Research
Volume370
Issue number2
DOIs
Publication statusPublished - Sep 15 2018
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Cell Biology

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