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

Yang Du, Marie Yang, Wei Wei, Hoang Dinh Huynh, Joachim Herz, Alan Saghatelian, Yihong Wan

Research output: Contribution to journalArticle

12 Citations (Scopus)

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.

Original languageEnglish (US)
Article number2011
JournalNature Communications
Volume3
DOIs
StatePublished - 2012

Fingerprint

lipoproteins
secretions
macrophages
milk
Nursing
Macrophages
Platelet Activating Factor
platelets
Milk
Inflammation
deletion
Macrophage-Activating Factors
Mothers
Mammals
anemias
Phospholipases A2
Alopecia
Immunologic Factors
mammals
Toxicity

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • Chemistry(all)
  • Physics and Astronomy(all)

Cite this

Macrophage VLDL receptor promotes PAFAH secretion in mother's milk and suppresses systemic inflammation in nursing neonates. / Du, Yang; Yang, Marie; Wei, Wei; Huynh, Hoang Dinh; Herz, Joachim; Saghatelian, Alan; Wan, Yihong.

In: Nature Communications, Vol. 3, 2011, 2012.

Research output: Contribution to journalArticle

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