Malpuech-Brugère C, Kuryszko J, Nowacki W, Rock E, Rayssiguier Y, Mazur A
Unite Maladies Métaboliques et Micronutriments, INRA, St Genès Champanelle, France.
Magnes Res. 1998 Sep;11(3):161-9.
Dietary magnesium deficiency in rodents, and especially in rats, causes inflammation and leads to alterations in the immune response. One of the characteristics of magnesium deficiency in the rat is a marked enlargement of the spleen. Considering the importance of the spleen for the immune response, in this study we have evaluated histological, cytological and immunological changes in this organ of rats in early stages of this deficiency. For this purpose, male weaning Wistar rats were pair-fed with either control or magnesium-deficient diet, for 2, 4 or 8 days. Results indicate that after 8 days on the deficient diet rats presented clinical signs of inflammation, splenomegalia and leukocytosis. As shown by histometrical analysis, both the red and white spleen pulps of deficient rats displayed an increased incidence of polymorphonuclear leukocytes and macrophages in all studied stages of deficiency. Concomitantly, the relative number of lymphocytes decreased. This observation was confirmed by the analysis of the cell suspension obtained from the spleen. The greater number of adherent cells in the cell suspension from deficient rats provides an additional confirmation of the increased number of macrophages in the spleen of these rats. Analysis of lymphocyte populations demonstrated a reduced proportion of CD5+ and CD8+ cells after 8 days of deficiency. The reduction in the number of CD8+ cells in deficient rats could be related to the observed decrease in IFN-gamma concentration in the spleen homogenate. In short, this study shows that magnesium deficiency causes early cytological and immunological modifications in the spleen which appeared before macroscopical changes in this organ and before clinical symptoms of inflammation. These changes could be related to the altered immune response of deficient animals.
啮齿动物,尤其是大鼠,膳食中镁缺乏会引发炎症并导致免疫反应改变。大鼠镁缺乏的特征之一是脾脏明显肿大。鉴于脾脏对免疫反应的重要性,在本研究中,我们评估了大鼠在这种缺乏症早期阶段该器官的组织学、细胞学和免疫学变化。为此,将雄性断奶Wistar大鼠成对饲养,分别给予对照饮食或缺镁饮食,持续2、4或8天。结果表明,在缺镁饮食8天后,大鼠出现炎症的临床症状、脾肿大和白细胞增多。组织计量学分析显示,在所有研究的缺乏阶段,缺镁大鼠的脾脏红髓和白髓中多形核白细胞和巨噬细胞的发生率均增加。与此同时,淋巴细胞的相对数量减少。从脾脏获得的细胞悬液分析证实了这一观察结果。缺镁大鼠细胞悬液中贴壁细胞数量更多,进一步证实了这些大鼠脾脏中巨噬细胞数量增加。淋巴细胞群体分析表明,缺乏8天后CD5+和CD8+细胞的比例降低。缺镁大鼠CD8+细胞数量的减少可能与脾脏匀浆中干扰素-γ浓度的降低有关。简而言之,本研究表明,镁缺乏会导致脾脏早期的细胞学和免疫学改变,这些改变在该器官出现宏观变化之前以及炎症临床症状出现之前就已出现。这些变化可能与缺镁动物免疫反应改变有关。