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束缚应激会在白细胞介素-10基因敲除小鼠中诱发并加剧肠道炎症。

Restraint stress induces and exacerbates intestinal inflammation in interleukin-10 deficient mice.

作者信息

Koh Seong-Joon, Kim Ji Won, Kim Byeong Gwan, Lee Kook Lae, Kim Joo Sung

机构信息

Seong-Joon Koh, Ji Won Kim, Byeong Gwan Kim, Kook Lae Lee, Department of Internal Medicine, Seoul National University Boramae Hospital, Seoul National University College of Medicine, Seoul 110-744, South Korea.

出版信息

World J Gastroenterol. 2015 Jul 28;21(28):8580-7. doi: 10.3748/wjg.v21.i28.8580.

Abstract

AIM

To investigate the effects of restraint stress on chronic colitis in interleukin (IL)-10 deficient (IL-10(-/-)) mice.

METHODS

The first experiment compared the effect of restraint stress on the development of intestinal inflammation in wild-type and IL-10(-/-) mice. Both wild-type and IL-10(-/-) mice were physically restrained in a well-ventilated, 50 cm(3) conical polypropylene tube for 2 h per day for three consecutive days. The second experiment was performed to assess the effect of restraint stress on exacerbation of colitis induced by piroxicam in IL-10(-/-) mice. The IL-10(-/-) mice were exposed to restraint stress for 2 h per day for 3 consecutive days, and then treated with piroxicam for 4 d at a dose of 200 ppm administered in the rodent chow.

RESULTS

In the first experiment, none of the wild-type mice with or without restraint stress showed clinical and histopathological abnormality in the gut. However, IL-10(-/-) mice exposed to restraint stress exhibited histologically significant intestinal inflammation as compared to those without restraint stress. In the second experiment, restraint stress significantly reduced body weight and increased the severity of intestinal inflammation assessed by histopathologic grading in IL-10(-/-) mice. Colonic IL12p40 mRNA expression was strongly increased in mice exposed to restraint stress.

CONCLUSION

This novel animal model could be useful in future study of psychological stress in the pathogenesis of inflammatory bowel disease.

摘要

目的

研究束缚应激对白细胞介素(IL)-10基因缺陷(IL-10(-/-))小鼠慢性结肠炎的影响。

方法

第一个实验比较束缚应激对野生型和IL-10(-/-)小鼠肠道炎症发展的影响。野生型和IL-10(-/-)小鼠均被物理束缚于通风良好的50立方厘米锥形聚丙烯管中,每天2小时,连续3天。第二个实验旨在评估束缚应激对吡罗昔康诱导的IL-10(-/-)小鼠结肠炎加重的影响。IL-10(-/-)小鼠连续3天每天接受2小时的束缚应激,然后以200 ppm的剂量在啮齿动物饲料中给予吡罗昔康治疗4天。

结果

在第一个实验中,无论有无束缚应激,野生型小鼠在肠道均未表现出临床和组织病理学异常。然而,与未受束缚应激的IL-10(-/-)小鼠相比,受束缚应激的IL-10(-/-)小鼠在组织学上表现出明显的肠道炎症。在第二个实验中,束缚应激显著降低了IL-10(-/-)小鼠的体重,并通过组织病理学分级评估增加了肠道炎症的严重程度。受束缚应激的小鼠结肠IL12p40 mRNA表达强烈增加。

结论

这种新的动物模型可能有助于未来研究心理应激在炎症性肠病发病机制中的作用。

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