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Antibodies in milk have to survive not one but two arduous journeys intact,
- First, they have to be transported intact across the epithelial cells that line the breast tissue lumen to get into milk.
- Second, in order to be useful (functional), they need to be able to withstand and emerge intact from the stomach’s acidic environment during their transit through the baby’s GI tract.
Breast milk contains not just any antibody but specialized antibodies designed to survive these two challenges.
Antibody composition in human milk is very different from its serum counterpart. Where IgM and IgG dominate serum with little IgA, the latter, specifically secretory IgA, is the most abundant antibody in human milk (1).
Secretory IgA dominates external secretions. Specialized plasma cells secrete it and a specialized process complete with a special receptor, the polymeric Ig receptor, transports this antibody intact across the mammary epithelial cells and into the breast tissue lumen to be excreted in milk, a process similar in its details to the way sIgA makes its way into the GI tract and upper respiratory tract lumen to bind and neutralize any pathogen-derived antigens found there to keep them out of the body (below from 2).
So important is secretory IgA in human milk that on average, concentrations of as much as 0.5 grams per day are maintained during the first year of lactation (3).
In fact, human milk and its earliest manifestation, colostrum, should be renamed specific transporter of secretory IgA, so abundant are these secretions in this one particular type of antibody (below from 4).
No surprise then that sIgA also survives intact its transit through the baby’s stomach (Below from 5, emphasis mine).
“IgA in milk is principally in the form of secre tory IgA (sIgA), which serves as a first line of mucosal defense. Maternal supply of sIgA is important as infant intestinal IgA production does not begin until several months of age, and even at 1 year of age serum IgA levels are only 20% of adult levels [22]. Although the extent to which antibodies are absorbed in early life remains controversial, it is most likely mod est, except perhaps in preterm infants [23–25]. Unlike other antibody isotypes, secretory IgA is resistant to degradation in the protease-rich external environments of mucosal surfaces, and the majority of ingested sIgA survives passage through the intestinal tract intact for at least the first year of life, providing mucosal protection in spite of the increasing surface area of the GI tract [26,27].”
The idea that the mother passively transfers immunity in the form of antibodies in milk to a newborn took root from studies in the 1930s that found that breast-feeding but not artificial (bottle) feeding prevented a variety of GI tract and respiratory infections in infants (6). Later studies confirmed this and showed IgA from mother’s milk appeared intact and functional in breast-fed infants (7, 8) and decades of subsequent research allows the following summaries.
Below from 9.
“Through the enteromammaric link the mother produces in her mammary glands large amounts of specific SIgA antibodies against the microbial and food antigens she has met in her previous life. These stable milk SIgA antibodies protect the mucosal membranes of the breastfed offspring efficiently and without inducing inflammation as occurs with tissue defense.”
Below from 10.
“…the protective value of breast-feeding is highlighted in relation to mucosal infections, particularly in the developing countries. At least 90% of microorganisms infecting humans, use the mucosae as portals of entry; such pathogens are a major killer of children below the age of 5 years, being responsible for more than 14 million deaths annually.”
Bibliography
1. Brandtzaeg, Per. “The mucosal immune system and its integration with the mammary glands.” The Journal of pediatrics 156.2 (2010): S8-S15.
2. Brandtzaeg, Per. “Secretory IgA: designed for anti-microbial defense.” Frontiers in immunology 4 (2013): 222. Secretory IgA: Designed for Anti-Microbial Defense
3. Weaver, Lawrence T., et al. “Human milk IgA concentrations during the first year of lactation.” Archives of disease in childhood 78.3 (1998): 235-239. https://adc.bmj.com/content/archdischild/78/3/235.full.pdf
4. Wheeler, Thomas T., et al. “Immune components of colostrum and milk—a historical perspective.” Journal of mammary gland biology and neoplasia 12.4 (2007): 237-247. http://colostrumscience.org/wp-content/uploads/2016/07/Wheeler-2007-milk-immmune-factors.pdf
5. Cerini, Chiara, and Grace M. Aldrovandi. “Breast milk: proactive immunomodulation and mucosal protection against viruses and other pathogens.” Future Virology 8.11 (2013): 1127-1134.
6. Grulee, Clifford G., Heyworth N. Sanford, and Paul H. Herron. “Breast and artificial feeding: influence on morbidity and mortality of twenty thousand infants.” Journal of the American Medical Association 103.10 (1934): 735-739.
7. Ogra, S. S., D. Weintraub, and Pearay L. Ogra. “Immunologic aspects of human colostrum and milk: III. Fate and absorption of cellular and soluble components in the gastrointestinal tract of the newborn.” The Journal of Immunology 119.1 (1977): 245-248. https://www.jimmunol.org/content/jimmunol/119/1/245.full.pdf
8. Weaver, L. T., et al. “The ontogeny of serum IgA in the newborn.” Pediatric Allergy and Immunology 2.2 (1991): 72-75.
9. Hanson, Lars A. “Breastfeeding provides passive and likely long-lasting active immunity.” Annals of Allergy, Asthma & Immunology 81.6 (1998): 523-537.
10. Brandtzaeg, Per. “Mucosal immunity: integration between mother and the breast-fed infant.” Vaccine 21.24 (2003): 3382-3388. http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.515.1530&rep=rep1&type=pdf