Session 1: Feeding and infant development Breast-feeding and immune function

Abstract

The newborn receives, via the placenta, maternal IgG antibodies against the microbes present in its surroundings, but such antibodies have a pro-inflammatory action, initiating the complement system and phagocytes. Although the host defence mechanisms of the neonate that involve inflammatory reactivity are somewhat inefficient, this defence system can still have catabolic effects. Breast-feeding compensates for this relative inefficiency of host defence in the neonate by providing considerable amounts of secretory IgA antibodies directed particularly against the microbial flora of the mother and her environment. These antibodies bind the microbes that are appearing on the infant's mucosal membranes, preventing activation of the pro-inflammatory defence. The major milk protein lactoferrin can destroy microbes and reduce inflammatory responses. The non-absorbed milk oligosaccharides block attachment of microbes to the infant's mucosae, preventing infections. The milk may contain anti-secretory factor, which is anti-inflammatory, preventing mastitis in mothers and diarrhoea in infants. Numerous additional factors in the milk are of unknown function, although IL-7 is linked to the larger size of the thymus and the enhanced development of intestinal Tgd lymphocytes in breast-fed compared with non-breast-fed infants. Several additional components in the milk may help to explain why breast-feeding can reduce infant mortality, protecting against neonatal septicaemia and meningitis. It is therefore important to start breast-feeding immediately. Protection is also apparent against diarrhoea, respiratory infections and otitis media. There may be protection against urinary tract infections and necrotizing enterocolitis, and possibly also against allergy and certain other immunological diseases, and tumours. In conclusion, breast-feeding provides a very broad multifactorial anti-inflammatory defence for the infant.

Protective effect of breastfeeding against childhood leukemia in Zhejiang Province, P. R. China: a retrospective case-control study

“…Because of the use of formula, the baby’s gut microorganisms are altered, which affects the immune system’s response to pathogens [23–26]. A great number of natural-killer cells, suggesting a more mature immune system, have been found in breastfed infants than in formula-fed infants [27]. In addition, the pH level (hydrogen ion concentration, which can activate pepsin and promote protein digestion and absorption) in the stomach of breastfed children is better for the promotion of the protein-lipid α-lactalbumin, which induces apoptosis like death of tumor cells [28,29].…”

Changes in immunomodulatory constituents of human milk in response to active infection in the nursing infant

“…sIgA is secreted from mammary lymphoid cells that probably originate from B lymphocytes migrating from the gastrointestinal tract to the mammary gland (4). Only a small portion of sIgA is secreted from macrophages containing this antibody.…”

“…In addition to transfer of immunoglobulin G to the fetus through the placenta, breastfeeding constitutes an important immunological support that the mammalian mother can provide to her relatively immunocompromised offspring against infections during the first months of life (2-6). The immune system in human milk includes secretory immunoglobulin A (sIgA), immunoglobulin G, free fatty acids, monoglycerides, proteins such as lactoferrin, lactalbumin, glycans, nonabsorbed oligosaccharides, exosomes, immunomodulators such as cytokines, nucleic acids, antioxidants, and immune cells such as macrophages, neutrophils, and lymphocytes (1,4,5,(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17). All these immunologic milk constituents interact together and with the newborn's gut directly or indirectly (e.g., by changing the gut flora) to increase immunity against infection, and probably also contribute to the maturation and efficiency of the newborn immune system (5,6).…”

Human milk glycosaminoglycans inhibit in vitro the adhesion of Escherichia coli and Salmonella fyris to human intestinal cells

“…As already demonstrated for other human milk (oligo)saccharides, exogenous GAGs have shown the ability as competitive inhibitors of bacterial adhesion, among which heparin has been studied most (3,23). As concerns the possible physiological role of GAGs in the gastrointestinal tract of breast-fed newborns, it is important to underline that undigested GAGs reach the small intestine because there are no specific enzymes present on the intestinal wall able to degrade them.…”