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Lactose in human breast milk an inducer of innate immunity with implications for a role in intestinal homeostasis. | LitMetric

AI Article Synopsis

  • Newborns rely on their innate immune system for protection against infections since their adaptive immune system isn't fully developed yet.
  • A factor from human milk, identified as lactose, can induce the gene (CAMP) responsible for producing the antimicrobial peptide LL-37 in colonic cells, suggesting lactose plays a role in enhancing immune defense.
  • Lactose's immune-boosting effect works through the p38 pathway and shows a synergistic effect with compounds like butyrate, highlighting its potential in protecting the neonatal gut and influencing infant microbiota.

Article Abstract

Postpartum, infants have not yet established a fully functional adaptive immune system and are at risk of acquiring infections. Hence, newborns are dependent on the innate immune system with its antimicrobial peptides (AMPs) and proteins expressed at epithelial surfaces. Several factors in breast milk are known to confer immune protection, but which the decisive factors are and through which manner they work is unknown. Here, we isolated an AMP-inducing factor from human milk and identified it by electrospray mass spectrometry and NMR to be lactose. It induces the gene (CAMP) that encodes the only human cathelicidin LL-37 in colonic epithelial cells in a dose- and time-dependent manner. The induction was suppressed by two different p38 antagonists, indicating an effect via the p38-dependent pathway. Lactose also induced CAMP in the colonic epithelial cell line T84 and in THP-1 monocytes and macrophages. It further exhibited a synergistic effect with butyrate and phenylbutyrate on CAMP induction. Together, these results suggest an additional function of lactose in innate immunity by upregulating gastrointestinal AMPs that may lead to protection of the neonatal gut against pathogens and regulation of the microbiota of the infant.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3542196PMC
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0053876PLOS

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