Mucosal immunity.
Mucosal defense is provided by a number of host factors countering the specific virulence factors of the many microorganisms infecting the mucous membranes. Secretory IgA antibodies presumably play an important role. Increase of the sIgA antibodies may most advantageously be attained by parenteral immunization, following mucosal priming. This was demonstrated in a rat model, where it was also noted that antigen injection into PP induced high milk IgA antibody levels. In man, parenteral vaccination against polio increased the sIgA antibody levels in the milk of mothers previously exposed naturally to the poliovirus. The response was relatively short-lived. In the previously unexposed, there was little or no response. By contrast peroral immunization with live poliovirus vaccine did not increase, or even decrease, the milk sIgA poliovirus antibody levels. Although salivary sIgA antibodies against antigens of colonizing E. coli appear during the first days of life, they are slow to increase. This deficiency is richly compensated for by all the sIgA antibodies that are provided the baby through the milk. No transfer of dimeric IgA into the milk could be shown in lactating rats, in contrast to what has been reported in mice. There is no evidence for a contribution to milk sIgA from serum in man. Close to parturition, human milk often contains some 7S IgA and various sizes of free SC, in addition to the dominating 11S sIgA. A few days later there is almost exclusively monomeric SC and 11S sIgA. IgG antibodies also play a role at the mucosal level. IgG2 antibodies against the bacterial polysaccharide capsule are as slow to appear as sIgA in ontogeny, possibly explaining the prevalence of infections with encapsulated bacteria and the poor response to polysaccharide vaccines in early childhood. Other defense factors preventing infections by way of mucous membranes may be important. Thus, oligosaccharides present in human milk seem to specifically prevent pneumococcal attachment to retropharyngeal cells. This anti-attachment capacity, in addition to that provided by milk and salivary IgA antibodies, may explain why breast-fed babies have less otitis media than formula-fed ones.
D000328:Adult; D000818:Animals; D000907:Antibodies, Bacterial / Q000096:biosynthesis; D000921:Antibody-Producing Cells / Q000276:immunology; D000941:Antigens / Q000276:immunology; D000942:Antigens, Bacterial / Q000276:immunology; D000954:Antigens, Surface; D002648:Child; D005260:Female; D006801:Humans; D007114:Immunization; D007070:Immunoglobulin A / Q000096:biosynthesis*; D007071:Immunoglobulin A, Secretory / Q000032:analysis / Q000096:biosynthesis; D007074:Immunoglobulin G / Q000096:biosynthesis; D007075:Immunoglobulin M / Q000096:biosynthesis; D007231:Infant, Newborn; D007413:Intestinal Mucosa / Q000276:immunology*; D007419:Intestinal Secretions / Q000276:immunology*; D051379:Mice; D008895:Milk, Human / Q000276:immunology; D019081:O Antigens; D011247:Pregnancy; D051381:Rats
D000907:Antibodies, Bacterial; D000941:Antigens; D000942:Antigens, Bacterial; D000954:Antigens, Surface; D007070:Immunoglobulin A; D007071:Immunoglobulin A, Secretory; D007074:Immunoglobulin G; D007075:Immunoglobulin M; C030659:K antigens; D019081:O Antigens