| Summary: | 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 receptor (VLDLR) deletion in mice causes the production of defective milk containing diminished level of platelet-activating factor acetylhydrolase (PAFAH). As a consequence, the nursing neonates suffer from alopecia, anemia and growth retardation owing to elevated levels of pro-inflammatory platelet-activating factors (PAFs). VLDLR 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 VLDLR in suppressing inflammation by maintaining macrophage PAFAH secretion, but also identify the maternal VLDLR as a key genetic program that ensures milk quality and protects the newborns.
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