Stat6 dependent goblet cell hyperplasia during intestinal nematode infection
Stat6 dependent goblet cell hyperplasia during intestinal nematode infection
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DOI：
10.1046/j.1365-3024.2001.00353.x
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发表时间：
2001-01-01
影响因子：
2.2
通讯作者：
Collins, SM
中科院分区：
文献类型：
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作者：
Khan, WI;Blennerhasset, P;Collins, SM
为了确定信号转导器和转录因子 6 (Stat6) 激活剂在线虫感染期间肠道杯状细胞增生发展中的作用，我们比较了 Stat6 缺陷 (Stat6 -/-) 小鼠中的杯状细胞数量与旋毛虫感染中野生型 (Stat6 +/+) 小鼠中产生的杯状细胞数量。野生型小鼠感染后杯状细胞的数量显着增加。然而，Stat6 -/- 未能产生感染诱导的杯状细胞增生，并且与 Stat6 +/+ 小鼠相比，在感染后第 14 天和 21 天，在 Stat6 -/- 小鼠中观察到杯状细胞数量显着减少。除了杯状细胞数量受到抑制之外。 Stat6-/- 小鼠产生 IL-4 和 IL-13 以及将寄生虫从肠道排出的能力严重受损。我们的研究清楚地表明了 Stat6 在伴随这种感染的肠杯状细胞增生中的重要作用。我们假设 Th2 细胞因子通过 Stat6 激活在线虫感染期间调节肠道杯状细胞增生的发展，并且杯状细胞数量的增加在宿主抵抗感染的保护性免疫中发挥重要作用。
To identify the role of signal transducer and activator of transcription factor 6 (Stat6) in the development of intestinal goblet cell hyperplasia during nematode infection, we compared the number of goblet cells in Stat6 deficient (Stat6 -/-) mice with that generated in wild-type (Stat6 +/+) mice in Trichinella spiralis infection. The number of goblet cells significantly increased with infection in wild-type mice. However, Stat6 -/- failed to generate infection-induced goblet cell hyperplasia and a significantly lower number of goblet cells was observed in Stat6 -/- mice on days 14 and 21 postinfection compared to Stat6 +/+ mice. In addition to suppressed goblet cell numbers. Stat6-/- mice exhibited severe impairment in their ability to produce IL-4 and IL-13 and to expel the parasites from the gut. Our study clearly shows an essential role of Stat6 in intestinal goblet cell hyperplasia which accompanies this infection. We postulate that Th2 cytokines regulate the development of goblet cell hyperplasia in gut during nematode infection via Stat6 activation and that the increased number of goblet cells plays an important role in host protective immunity against the infection.