Hanson L A, Ahlstedt S, Andersson B, Carlsson B, Cole M F, Cruz J R, Dahlgren U, Ericsson T H, Jalil F, Khan S R, Mellander L, Schneerson R, Edén C S, Söderström T, Wadsworth C
Ann N Y Acad Sci. 1983 Jun 30;409:1-21. doi: 10.1111/j.1749-6632.1983.tb26855.x.
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.
黏膜防御由多种宿主因素提供，这些因素可对抗感染黏膜的众多微生物的特定毒力因子。分泌型IgA抗体可能起着重要作用。在黏膜启动后，通过肠胃外免疫最有可能提高分泌型IgA抗体水平。这在大鼠模型中得到了证实，在该模型中还发现，将抗原注射到派伊尔结可诱导乳汁中IgA抗体水平升高。在人类中，针对脊髓灰质炎的肠胃外疫苗接种增加了先前自然接触过脊髓灰质炎病毒的母亲乳汁中的分泌型IgA抗体水平。这种反应持续时间相对较短。在先前未接触过的人群中，几乎没有反应。相比之下，口服活脊髓灰质炎疫苗并没有增加甚至降低了乳汁中脊髓灰质炎病毒的分泌型IgA抗体水平。虽然针对定居大肠杆菌抗原的唾液分泌型IgA抗体在生命的最初几天就会出现，但它们的增加速度较慢。通过乳汁提供给婴儿的所有分泌型IgA抗体充分弥补了这一不足。与小鼠的报道相反，在泌乳大鼠中未发现二聚体IgA向乳汁中的转移。没有证据表明人类血清对乳汁分泌型IgA有贡献。临近分娩时，人乳中除了占主导地位的11S分泌型IgA外，通常还含有一些7S IgA和各种大小的游离分泌片。几天后，几乎只剩下单体分泌片和11S分泌型IgA。IgG抗体在黏膜水平也发挥作用。针对细菌多糖荚膜的IgG2抗体在个体发育中出现的速度与分泌型IgA一样慢，这可能解释了幼儿期包膜细菌感染的普遍性以及对多糖疫苗反应不佳的原因。其他通过黏膜预防感染的防御因素可能也很重要。因此，人乳中存在的寡糖似乎能特异性地阻止肺炎球菌附着于咽后细胞。这种抗附着能力，除了乳汁和唾液IgA抗体提供的能力外，可能解释了母乳喂养的婴儿比配方奶喂养的婴儿患中耳炎的几率更低的原因。
