Why We Develop Food Allergies
Coached by breast milk and good bacteria, the immune system strives to learn the difference between food and pathogens before the first morsel crosses our lips
An infant floating in the womb enjoys warmth, nutrition and an environment free of microorganisms. During the birth process—even before she takes her first breath—a baby begins to encounter microbes and other foreign substances, collectively called antigens, that can stimulate her new immune system. Most of these immunological challenges take place on mucosal surfaces such as the gut and airways.
The first line of defense in a newborn's gut is the system of immune exclusion, which uses exported antibodies to bind germs and potentially harmful compounds on the mucosal surface. Antibodies coat the pathogens to prevent them from invading the gut wall, and they bind to unfamiliar cell fragments or macromolecules to regulate their passage into the body. The class of antibodies known as secretory immunoglobulin A(SIgA) is most responsible for immune exclusion; it is a nice antibody that is actively pumped out to the surface and seldom elicits inflammation when it goes to work.
New babies, however, produce little or no SIgA. They depend on other types of antibodies during the first vulnerable months of life, primarily residual IgG from the mother and small amounts of mucosal IgM. The only significant source of SIgA antibodies during this period is breast milk, which helps protect the newborn until her immune system is established. In developed countries, the child's ability to produce SIgA is quite variable, being completed between one and ten years of age. Babies in developing countries often establish secretory immunity much earlier, presumably because of greater exposure to stimulating microbes.
In addition to their job of binding up troublesome antigens, SIgA antibodies help the gut to develop by enhancing the barrier function of the epithelial lining. The gut mucosa of most infants matures during the first months of life. But in some children, the mucosal barrier remains inadequate for several years, and incomplete secretory immunity can contribute to the delay. Not surprisingly, genetically manipulated (knockout) mice that lack SIgA and SIgM have leaky mucosal membranes.
The SIgA system seems to be important in setting an individual's threshold for adverse reactions to food. The risk of food allergy is higher when the development of IgA-producing cells is retarded or when SIgA-dependent development of the gut barrier is insufficient. On the positive side, babies who breastfeed exclusively for at least the first four months appear to have fewer allergies. This effect may be the product of IgA-directed gut maturation, but human milk also contains immune cells, immune-regulating cytokines and growth factors that exert positive biological effects.