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Macrophage VLDL receptor promotes PAFAH secretion in mother's milk and suppresses systemic inflammation in nursing neonates

Author

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  • Yang Du

    (University of Texas Southwestern Medical Center)

  • Marie Yang

    (University of Texas Southwestern Medical Center)

  • Wei Wei

    (University of Texas Southwestern Medical Center)

  • Hoang Dinh Huynh

    (University of Texas Southwestern Medical Center)

  • Joachim Herz

    (University of Texas Southwestern Medical Center)

  • Alan Saghatelian

    (Harvard University)

  • Yihong Wan

    (University of Texas Southwestern Medical Center)

Abstract

Mother's milk is widely accepted as nutritious and protective to the newborn mammals by providing not only macronutrients but also immune-defensive factors. However, the mechanisms accounting for these benefits are not fully understood. Here we show that maternal very-low-density-lipoprotein (VLDL) receptor deletion in mice causes the production of defective milk containing diminished levels of platelet-activating factor acetylhydrolase (PAFAH). As a consequence, the nursing neonates suffer from alopecia, anaemia and growth retardation owing to elevated levels of pro-inflammatory platelet-activating factors. VLDL receptor deletion significantly impairs the expression of phospholipase A2 group 7 (Pla2g7) in macrophages, which decreases PAFAH secretion. Exogenous oral supplementation of neonates with PAFAH effectively rescues the toxicity. These findings not only reveal a novel role of VLDL receptor in suppressing inflammation by maintaining macrophage PAFAH secretion, but also identify the maternal VLDL receptor as a key genetic program that ensures milk quality and protects the newborns.

Suggested Citation

  • Yang Du & Marie Yang & Wei Wei & Hoang Dinh Huynh & Joachim Herz & Alan Saghatelian & Yihong Wan, 2012. "Macrophage VLDL receptor promotes PAFAH secretion in mother's milk and suppresses systemic inflammation in nursing neonates," Nature Communications, Nature, vol. 3(1), pages 1-8, January.
    • Handle: RePEc:nat:natcom:v:3:y:2012:i:1:d:10.1038_ncomms2011
    DOI: 10.1038/ncomms2011
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