Abstract
Human breast milk is well known as the ideal source of nutrition during early life, ensuring optimal growth during infancy and early childhood. Breast milk is also the source of many unique and dynamic bioactive components that play a key role in the development of the immune system. These bioactive components include essential microbes, human milk oligosaccharides (HMOs), immunoglobulins, lactoferrin and dietary polyunsaturated fatty acids. These factors all interact with intestinal commensal bacteria and/or immune cells, playing a critical role in establishment of the intestinal microbiome and ultimately influencing intestinal inflammation and gut health during early life. Exposure to breast milk has been associated with a decreased incidence and severity of necrotizing enterocolitis (NEC), a devastating disease characterized by overwhelming intestinal inflammation and high morbidity among preterm infants. For this reason, breast milk is considered a protective factor against NEC and aberrant intestinal inflammation common in preterm infants. In this review, we will describe the key microbial, immunological, and metabolic components of breast milk that have been shown to play a role in the mechanisms of intestinal inflammation and/or NEC prevention.
Highlights
Human breast milk is well known as the optimal source of nutrition during early life, as a result of a nutritional content that evolves with the needs of the growing infant [1,2]
This exaggerated inflammatory response has been implicated in the pathogenesis of necrotizing enterocolitis (NEC), a disease characterized by overwhelming intestinal inflammation and a major contributor to neonatal morbidity and mortality [19,22]
Intestinal inflammation has a vital role in the neonatal immune response, excessive inflammation may lead to decreased gastrointestinal function and injury
Summary
Human breast milk is well known as the optimal source of nutrition during early life, as a result of a nutritional content that evolves with the needs of the growing infant [1,2]. The preterm intestine exhibits high expression of Toll-like receptor 4 (TLR4), an immune receptor expressed on leukocyte membranes that recognize molecular patterns in potential pathogens and, in turn, upregulate and suppress genes that orchestrate an inflammatory response [20,21]. This exaggerated inflammatory response has been implicated in the pathogenesis of necrotizing enterocolitis (NEC), a disease characterized by overwhelming intestinal inflammation and a major contributor to neonatal morbidity and mortality [19,22]. NEC is an extreme example of intestinal inflammation, underpinning the importance of bioactive factors in human milk
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