A receptor on immune cells that protects nursing newborns from inflammation by ensuring the quality of the milk has been identified in a study published in Nature Communications. The work reveals a novel anti-inflammatory role for the lipoprotein receptor VLDLR and finds that it controls secretion of a protective enzyme from immune cells into mother’s milk.
Mother’s milk contains a range of nutrients and protective molecules, including the enzyme platelet-activating factor acetylhydrolase (PAFAH). PAFAH degrades an inflammatory lipid molecule called platelet-activating factor (PAF) in the blood of neonates while their immune system is not fully developed. VLDLR has so far mostly been studied in the context of lipid metabolism and brain development.
Yihong Wan and his team observed that mouse pups nursed by mothers that do not have VLDLR developed body-wide inflammation. The symptoms were caused by high levels of PAF in the pup’s blood due to a lack of PAFAH in the milk supplied by their mothers. The authors noted that the level of PAFAH in mother’s milk was controlled by VLDLR on immune cells called macrophages, which produce and secrete the enzyme after activation of the receptor.
The finding could shed new light on the causation of some inflammatory neonatal disorders and possibly on inflammatory diseases in adulthood known to be associated with PAF, such as Crohn’s disease, atherosclerosis or asthma.
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