Absence of lactobacilli containing glycolipids with the α-galactose epitope and the enhanced fucosylation of a receptor glycolipid GA1 in the digestive tracts of immune-deficient scid mice.
Absence of lactobacilli containing glycolipids with the α-galactose epitope and the enhanced fucosylation of a receptor glycolipid GA1 in the digestive tracts of immune-deficient scid mice.
复制标题
免疫缺陷 scid 小鼠消化道中不存在含有具有 α-半乳糖表位的糖脂的乳杆菌，并且受体糖脂 GA1 的岩藻糖基化增强。
作者：
Iwamori M;Tanaka K;Adachi S;Aoki D;Nomura T.
免疫缺陷scid小鼠消化道中的乳杆菌种类与对照小鼠不同，即鼠乳杆菌scid和L.根据它们的16 S-rRNA，johnsoniin对照小鼠，表明乳酸杆菌和宿主之间的共生关系是在免疫系统的压力下建立的。盲肠和结肠内容物富含L。scid小鼠的小肠松散，有强烈的酸味，导致腹泻，而L.约翰逊对照小鼠包括丰富的固体物质。乳酸菌糖脂可被免疫系统识别，TLC免疫染色显示乳酸菌的LacTetH-DG（Galα1 - 6 Gal α1 - 6 Gal α1-2Glcα1- 3 'DG）。在对照小鼠的胃、盲肠和结肠中检测到johnsonii，而在scid小鼠的胃、盲肠和结肠中未检测到johnsonii，其中L.与对照小鼠相比，JohnsonII增强超过4倍。因此，揭示了受体糖脂的结构修饰发生在乳杆菌和宿主之间建立共生关系的过程中。LacTetH-DG也对人具有免疫原性，因为存在针对它的天然抗体，并且与其结合的抗体与血型和物种相关的鞘糖脂的抗体相当。
The Lactobacillus species in the digestive tracts of immune-deficient scid mice was distinct from that in control mice,i.e. Lactobacillus murinusin scid andL. johnsoniiin control mice, according to their 16S-rRNA, indicating that a symbiotic relationship between lactobacilli and a host is established under pressure from the immune system. The caecal and colonal contents rich inL. murinusof scid mice were loose with a strong sour smell, resulting in diarrhoea, and those withL. johnsoniiin control mice included abundant solid materials. Lactobacillus glycolipids were revealed to be recognized by the immune system, and by TLC-immunostaining, LacTetH-DG (Galα1-6Galα1-6Galα1-2Glcα1-3’DG) ofL. johnsoniiwas detected in the stomach, caecum and colon of control mice, but not in those of scid ones, in which fucosylation of a receptor GA1 forL. johnsoniiwas enhanced more than 4-fold compared with in the control mice. Thus, structural modification of receptor glycolipids was revealed to occur in the process of establishment of a symbiotic relationship between lactobacilli and a host. LacTetH-DG was also immunogenic to human, because of the presence of natural antibodies against it, and the antibody binding to it was comparable to that of blood group- and species-related glycosphingolipids.