Apoptosis induced by a human milk protein

Research output: Contribution to journalArticle

Abstract

To the breast-fed infant, human milk is more than a source of nutrients; it furnishes a wide array of molecules that restrict microbes, such as antibodies, bactericidins, and inhibitors of bacterial adherence. However, it has rarely been considered that human milk may also contain substances bioactive toward host cells. While investigating the effect of human milk on bacterial adherence to a human lung cancer cell line, we were surprised to discover that the milk killed the cells. Analysis of this effect revealed that a component of milk in a particular physical state--multimeric alpha-lact-albumin--is a potent Ca(2+)-elevating and apoptosis-inducing agent with broad, yet selective, cytotoxic activity. Multimeric alpha-lactalbumin killed all transformed, embryonic, and lymphoid cells tested but spared mature epithelial elements. These findings raise the possibility that milk contributes to mucosal immunity not only by furnishing antimicrobial molecules but also by policing the function of lymphocytes and epithelium. Finally, analysis of the mechanism by which multimeric alpha-lactalbumin induces apoptosis in transformed epithelial cells could lead to the design of antitumor agents.

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Authors
Organisations
Research areas and keywords

Subject classification (UKÄ) – MANDATORY

  • Immunology in the medical area

Keywords

  • Animals, Apoptosis, Bacterial Adhesion, Breast Feeding, Calcium, Calcium-Transporting ATPases, Cattle, Cell Line, Cell Survival, Chromatin, Chromatography, Ion Exchange, Dogs, Electrophoresis, Polyacrylamide Gel, Embryo, Mammalian, Female, Humans, Infant, Lactalbumin, Lung Neoplasms, Lymphocytes, Milk Proteins, Milk, Human, Terpenes, Thapsigargin, Tumor Cells, Cultured
Original languageEnglish
Pages (from-to)8064-8068
Number of pages5
JournalProceedings of the National Academy of Sciences
Volume92
Issue number17
Publication statusPublished - 1995 Aug 15
Publication categoryResearch
Peer-reviewedYes