Morphological and immune response alterations in the intestinal mucosa of the mouse after short periods on a low-magnesium diet.

The importance of Mg for the immune function is well recognized; however, there is no information available about the effect of Mg intake on the modulation of local immune response in the intestine. Thus, in the present study the hypothesis that short periods of Mg deprivation can affect intestinal mucosa and local immune response was tested. For this purpose, OF1 female mice were fed a semipurified diet (1000 mg Mg/kg diet). For 3 d before immunization and 1 d after, half of the animals were fed a Mg-deficient diet (30 mg Mg/kg diet), three immunizations per os were performed every 3 weeks with Escherichia coli producing the CS31A capsule-like protein (1010 or bacteria per animal). Mice were killed 10 d after the last immunization. The level of specific anti CS31A immunoglobulin (Ig) G and IgA in the serum and secretory IgA in the intestinal secretions and faeces were measured by ELISA. The results indicated that administration of a high dose of immunogen with a low-Mg diet led to lower specific IgA levels in the intestinal mucus and serum. Administration of a low dose of immunogen with a low-Mg diet led to lower IgA and IgG levels in the serum and secretory IgA coproantibodies. To assess alterations of intestinal mucosa caused by a low-Mg diet for a short period, histological and scanning electron microscopy analyses were performed on samples from mice (not submitted to the vaccination protocol) after 3 d on the Mg-deficient diet. These analyses showed several alterations, suggesting perturbations in the growth of the intestinal mucosa. These changes were accompanied by modifications in the expression of several genes involved in cell growth and stress response. From this present work, it may be concluded that short periods of Mg deprivation can affect the intestinal mucosa and local immune response of the intestine.

Stress protein expression cDNA array study supports activation of neutrophils during acute magnesium deficiency in rats.

Recent studies underline the importance of the immunoinflammatory processes in the pathology of acute magnesium (Mg)-deficiency. The aim of this study was to assess the effect of acute experimental Mg-deficiency in the rat on neutrophil activity. Weaning male Wistar rats were fed either a Mg-deficient or a control diet for 8 days. In this experiment, we measured neutrophil respiratory burst by chemiluminescence; then, to examine the molecular events associated with acute Mg-deficiency, we applied cDNA array technology to define the transcription response in neutrophils of Mg-deficient rats in comparison with controls. In Mg-deficient rats, the characteristic inflammatory response was accompanied by a marked increase in the number of neutrophils. Moreover, as shown by chemiluminescence studies, basal neutrophil activity from Mg-deficient rats was significantly elevated when compared to neutrophils from control rats. Moreover, the chemiluminescence of neutrophils from Mg-deficient rats was significantly higher than that of control rats following phorbol myristate acetate or opsonized zymosan activation. Using cDNA array which includes 207 known rat genes of stress proteins, 102 genes were found to be expressed in neutrophils. Among expressed genes, 78 per cent of genes were found to be expressed more than twofold in neutrophils from Mg-deficient rats compared to control rats. Acute Mg-deficiency was characterized by an induction of genes encoding for proteins involved in apoptosis, heat shock proteins, protein belonging to the cytoskeleton, proteins implicated as stress response regulators and effectors and enzyme implicated in thromboxane synthesis. Then, this experimental strategy allowed to identify a series of genes implicated in the immunoinflammatory process of Mg-deficiency.