Enhanced expression of fucosyl GA1 in the digestive tract of immune-deficient scid, nude and IgR (-/-) mice.

Enhanced expression of fucosyl GA1 in the digestive tract of immune-deficient scid, nude and IgR (-/-) mice.
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免疫缺陷 scid、裸鼠和 IgR (-/-) 小鼠消化道中岩藻糖基 GA1 的表达增强。

DOI:
10.1093/jb/mvt087
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发表时间:
2013
期刊:
J. Biochem.
影响因子:
--
通讯作者:
et al.
et al.
中科院分区:
--
文献类型:
--
作者:
Masao Iwamori;et al.

文献摘要

相似文献

小鼠肠上皮细胞中GA 1的岩藻糖基化通过α 1,2-岩藻糖基转移酶的转录诱导沿着细菌感染而发生,但其机制尚未明确表征,即其是否是由于对细菌的免疫应答或细菌对宿主的遗传操纵而诱导的。因此,我们分析了免疫缺陷scid、裸小鼠和pIgR(−/−)小鼠消化道中岩藻糖基GA 1(FGA 1)的表达和岩藻糖基转移酶活性。与相同SPF条件下饲养的对照小鼠相比,免疫缺陷小鼠的FGA 1含量和α 1,2-岩藻糖基转移酶活性显着增加,表明免疫系统不参与α 1,2-岩藻糖基转移酶基因的诱导。免疫缺陷小鼠肠内容物中FGA 1的总量高于对照小鼠,反映了FGA 1合成的增强。此外,在免疫缺陷小鼠和对照小鼠中,MRS琼脂平板上生长的主要粪便细菌不同,如下所示:scid和pIgR(−/−)小鼠为鼠乳杆菌,对照小鼠为约氏乳杆菌,裸鼠为粪肠球菌,对照小鼠为加氏乳球菌,表明肠道乳酸杆菌的改变部分参与了α 1,2-岩藻糖基转移酶的诱导。
Fucosylation of GA1 in murine intestinal epithelia occurs through transcriptional induction of α1,2-fucosyltransferase along with bacterial infection, but the mechanism has not been clearly characterized as to whether it is induced as a result of an immune response to bacteria or of genetic manipulation of the host by bacteria. Accordingly, we analysed the expression of fucosyl GA1 (FGA1) and fucosyltransferase activity in the digestive tracts of immune-deficient scid, nude and pIgR(−/−) mice. In comparison with those in control mice bred under the same SPF circumstances, the amount of FGA1 and the α1,2-fucosyltransferase activity were significantly increased in the immune-deficient mice, indicating that the immune system is not involved in induction of the α1,2-fucosyltransferase gene. Reflecting the enhanced synthesis of FGA1, the total amounts of FGA1 in the intestinal contents of immune-deficient mice were higher than those in control mice. Also, the major faecal bacteria grown on a MRS agar plate were different in immune-deficient and control mice as follows,Lactobacillus murinusfor scid and pIgR(−/−) mice, andLactobacillus johnsoniifor their control, andEnterococcus faecalisfor nude mice andLactococcus garvieaefor the control, indicating that an alteration in the intestinal lactobacilli is partly involved in the induction of α1,2-fucosyltransferase.