Kawai Yuichi, Yamauchi Junko, Soga Koichi, Yamada Minoru, Uchikawa Ryuichi, Tegoshi Tatsuya, Arizono Naoki
Department of Medical Zoology, Kyoto Prefectural University of Medicine, Kyoto, Japan.
APMIS. 2007 Mar;115(3):210-7. doi: 10.1111/j.1600-0463.2007.apm_510.x.
To determine how T cells of thymic origin regulate the intestinal mucous response induced by nematode infection, mucin production and goblet cell-specific secretory peptide expression were examined in euthymic rnu/+ and athymic rnu/rnu rats infected with the nematode Nippostrongylus brasiliensis. Euthymic rats showed transient goblet cell hyperplasia and upregulation of mucin production, which returned to preinfection levels by 21 days postinfection, when nematodes had been rejected from the intestine. In athymic rats, which failed to reject nematodes, goblet cell hyperplasia and accelerated mucin production continued at least until 21 days postinfection. Gene transcription of mucin-core peptide (MUC)-2 and -3 and trefoil factor (TFF)-2 and -3 in the jejunal epithelium was upregulated parallel to the levels of goblet cell hyperplasia in both euthymic and athymic rats. On the other hand, resistin-like molecule (Relm)beta, sialyltransferase Siat4c and sulfotransferase 3ST1 showed significantly higher transcription levels in euthymic than in athymic rats at 7 and/or 10 days postinfection. These results suggest that the induction of intestinal mucin production occurs without the activation of thymus-derived T cells, while the expression of Relmbeta, Siat4c and 3ST1 in the intestinal epithelial cells seems to be regulated at least partly by thymus-dependent mechanisms.
为了确定胸腺来源的T细胞如何调节线虫感染诱导的肠道黏液反应,我们在感染巴西日圆线虫的正常胸腺rnu/+大鼠和无胸腺rnu/rnu大鼠中检测了黏蛋白产生和杯状细胞特异性分泌肽表达。正常胸腺大鼠表现出短暂的杯状细胞增生和黏蛋白产生上调,在感染后21天,线虫从肠道被清除时,其恢复到感染前水平。在未能清除线虫的无胸腺大鼠中,杯状细胞增生和黏蛋白产生加速至少持续到感染后21天。在正常胸腺和无胸腺大鼠中,空肠上皮中黏蛋白核心肽(MUC)-2和-3以及三叶因子(TFF)-2和-3的基因转录与杯状细胞增生水平平行上调。另一方面,在感染后7天和/或10天,抵抗素样分子(Relm)β、唾液酸转移酶Siat4c和硫酸转移酶3ST1在正常胸腺大鼠中的转录水平显著高于无胸腺大鼠。这些结果表明,肠道黏蛋白产生的诱导在没有胸腺来源T细胞激活的情况下发生,而肠道上皮细胞中Relmβ、Siat4c和3ST1的表达似乎至少部分受胸腺依赖机制调节。