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The Role of Human Milk Secretory IgA in Protecting Infants from Bacterial Enteritis
Human milk: Defense against infection
An unborn baby makes no IgG antibody and only slowly starts producing it after birth. However, starting at about the sixth month of pregnancy, the fetus starts to receive maternal IgG antibody through the placenta. This increases during the last trimester of pregnancy until at term birth the baby has a level of IgG, the main class of antibody in the circulation, equivalent to that of the mother. The baby does not get any maternal IgM, IgA or IgE as they do not cross the placenta, so if IgM is found it may suggest the baby has encountered an infection in utero.
As a veteran neonatal nurse and lactation consultant, I am often asked by parents to explain how the antibodies found in breastmilk work to protect their babies. Published research on immunology is extremely technical and difficult to understand, and unfortunately, the information that is readily available especially on social media contains a lot of false and conflicting information. Our immune system is very complex, but generally speaking, it is responsible for fighting off both germs that enter our bodies from our environment, and also for protecting us from diseases like cancer that occur within our bodies. I will be focusing on how the immune system fights off germs, which it does by producing antibodies.
Human breast milk contains an array of factors with anti-infectious potential, such as immunoglobulins especially secretory IgA , oligosaccharides and glycoproteins with anti-adhesive capacity, and cytokines. Breast-feeding is associated with protection from the following infections or infection-related conditions: gastroenteritis, upper and lower respiratory tract infection, acute otitis media, urinary tract infection, neonatal septicaemia and necrotizing enterocolitis. Some of the protective effects may derive from an altered mucosal colonization pattern in the breast-fed infant. In other instances breast-fed infants develop less symptoms to the same microbe which causes disease in the bottle-fed infant. An example of an altered colonization pattern is that breast-fed infants have less P-fimbriated, but more type 1-fimbriated E.