Kang Woodae, Kudsk Kenneth A
Department of Surgery, The University of Wisconsin - Madison, Madison, Wisconsin, USA.
JPEN J Parenter Enteral Nutr. 2007 May-Jun;31(3):246-58. doi: 10.1177/0148607107031003246.
Our understanding of the common mucosal immune system derives from animal studies. Antigen-sensitized lymphocytes in the gut-associated lymphoid tissue (GALT) migrate via the blood to mucosal tissues to generate the mucosal-associated lymphoid tissue (MALT). In these sites, B cells differentiate into plasma cells and produce antigen-specific secretory IgA, the principal specific immune antiviral and antibacterial defense of moist mucosal surfaces. Responses to oral intake seem necessary to actively maintain this system in health. Experimentally, lack of enteral stimulation with parenteral feeding alters GALT and MALT size and function. These alterations disturb intestinal and extraintestinal mucosal immunity.
This review is an overview of current and classical studies demonstrating the human mucosal immune system and interactions with nutrition.
Human evidence of the mucosal immune system exists, although most data are indirect. Gut stimulation after oral intake induces a generalized immune response in the human MALT through a mucosal-immune network. Examples include neonatal development of GALT influenced by enteral feeding, the presence of antigen-specific IgA and antigen-specific IgA-secreting plasma cells in distant mucosal effector sites such as the breast after gut luminal antigen exposure, and isolation of IgA-producing cells from circulating blood.
It is unlikely that clinical studies will ever completely define the effect of route of feeding in all patient populations. This may be possible, however, if investigators understand, define and characterize nutrition-dependent immunologic mechanisms, allowing clinicians to examine clinical responses to nutrition in specific patient populations. This might allow generation of new approaches to protect mucosal immunity.
我们对共同黏膜免疫系统的认识源于动物研究。肠道相关淋巴组织（GALT）中经抗原致敏的淋巴细胞通过血液迁移至黏膜组织，以生成黏膜相关淋巴组织（MALT）。在这些部位，B细胞分化为浆细胞并产生抗原特异性分泌型IgA，这是湿润黏膜表面主要的特异性免疫抗病毒和抗菌防御物质。对经口摄入的反应似乎是积极维持该系统健康所必需的。在实验中，肠外营养缺乏肠内刺激会改变GALT和MALT的大小及功能。这些改变会干扰肠道和肠外黏膜免疫。
本综述概述了当前及经典研究，这些研究展示了人类黏膜免疫系统及其与营养的相互作用。
尽管大多数数据是间接的，但存在人类黏膜免疫系统的证据。经口摄入后肠道刺激通过黏膜免疫网络在人类MALT中诱导全身性免疫反应。实例包括肠内喂养对GALT新生儿发育的影响、肠道腔内抗原暴露后在远处黏膜效应部位（如乳腺）存在抗原特异性IgA及分泌抗原特异性IgA的浆细胞，以及从循环血液中分离出产生IgA的细胞。
临床研究不太可能完全确定所有患者群体中喂养途径的影响。然而，如果研究人员理解、界定并描述营养依赖的免疫机制，使临床医生能够在特定患者群体中研究营养的临床反应，那么这或许是可行的。这可能会催生保护黏膜免疫的新方法。
