Milk sIgA is not taken up by the infant's intestinal mucosa [148, 158] . In fact, gut closure in humans occurs before birth and little immunoglobulin is absorbed intact in the intestine after birth [148, 158] . However, the presence of sIgA in the intestinal lumen is part of the protective function of the epithelial barrier in the intestine [159] . Milk sIgA in the intestine will bind bacteria, toxins and other macromolecules, limiting their ability to bind to intestinal cells and thereby be transported through the mucosa to the lamina propria to cause a systemic immune response [160] . In adults of a pIgR-deficient strain of mice, which do not transport sIgA into the intestinal lumen, there is an increased serum IgA and IgG that react with commensal organisms and food antigens [161] . This may be occurring because sIgA is not being secreted into the intestinal lumen to participate in its role in immune exclusion (see section 6.3), and resulting in an increased uptake of food antigens and microbial antigens from the intestinal lumen which pass to the lamina propria and stimulate specific antibody responses [161] . Development of the GALT system is dependent on microbial stimulation [148, 158] . The microbe binding function of sIgA then modulates the early microbial colonization of the gastrointestinal tract and the interaction of those microbes with the developing neonatal immune system [148, 158, 160] .