Gay Jérôme, Moré Jean, Bueno Lionel, Fioramonti Jean
Neurogastroenterology and Nutrition Unit, INRA, 180 Chemin de Tournefeuille, BP 3, F-31931 Toulouse Cedex 9, France.
Brain Res. 2002 Jun 28;942(1-2):124-7. doi: 10.1016/s0006-8993(02)02652-5.
Intestinal infections often trigger functional bowel disorders. The nematode Nippostrongylus brasiliensis induces post-infective alterations mainly consisting in an intestinal mast cell hyperplasia. Mast cells contact vagal afferent nerve fibres. Therefore, it is possible that the anatomical sequels of intestinal nematode infection induce long term alterations in the mediation of afferent signals from the gut to the brain. To test this hypothesis, we examined hindbrain expression of Fos immunoreactivity following systemic cholecystokinin (CCK) administration in control rats and 35 days after N. brasiliensis infection. In controls, Fos was expressed in the area postrema and the nucleus of solitary tract. After infection, this expression was increased by 262 and 157%, respectively. We conclude that an intestinal infection, at least in this model, is followed by an enhancement of the activation of hindbrain sites by CCK.
肠道感染常引发功能性肠道疾病。巴西日圆线虫会诱发感染后的改变，主要表现为肠道肥大细胞增生。肥大细胞与迷走神经传入纤维接触。因此，肠道线虫感染的解剖学后果有可能会引起从肠道到大脑的传入信号传导长期改变。为验证这一假设，我们检测了对照大鼠经全身注射胆囊收缩素（CCK）后以及感染巴西日圆线虫35天后后脑Fos免疫反应性的表达情况。在对照组中，Fos在最后区和孤束核表达。感染后，该表达分别增加了262%和157%。我们得出结论，至少在这个模型中，肠道感染后CCK对后脑部位的激活作用增强。
