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Inflammatory response following acute magnesium deficiency in the rat
C Malpuech-Brugère1, W Nowacki, M Daveau
1Centre de Recherches en Nutrition Humaine, Unité Maladies Métaboliques et Micronutriments, INRA, Theix, St. Genès Champanelle, France.
Abstract:
The importance of inflammatory processes in the pathology of Mg deficiency has been recently reconsidered but the sequence of events leading to the inflammatory response remains unclear. Thus, the purpose of the present study was to characterize more precisely the acute phase response following Mg deficiency in the rat. Weaning male Wistar rats were pair-fed either a Mg-deficient or a control diet for either 4 or 8 days. The characteristic allergy-like crisis of Mg-deficient rats was accompanied by a blood leukocyte response and changes in leukocytes subpopulations. A significant increase in interleukin-6 (IL-6) plasma level was observed in Mg-deficient rats compared to rats fed a control diet. The inflammatory process was accompanied by an increase in plasma levels of acute phase proteins. The concentrations of alpha2-macroglobulin and alpha1-acid glycoprotein in the plasma of Mg-deficient rats were higher than in control rats. This was accompanied in the liver by an increase in the level of mRNA coding for these proteins. Moreover, Mg-deficient rats showed a significant increase in plasma fibrinogen and a significant decrease in albumin concentrations. Macrophages found in greater number in the peritoneal cavity of Mg-deficient rats were activated endogenously and appeared to be primed for superoxide production following phorbol myristate acetate stimulation. A high plasma level of IL-6 could be detected as early as day 4 for the Mg-deficient diet. Substance P does not appear to be the initiator of inflammation since IL-6 increase was observed without plasma elevation of this neuropeptide. The fact that the inflammatory response was an early consequence of Mg deficiency suggests that reduced extracellular Mg might be responsible for the activated state of immune cells.
Insights
Magnesium (Mg) deficiency triggers an early inflammatory response in rats, characterized by increased immune cells and inflammatory markers like interleukin-6 (IL-6). This suggests reduced extracellular Mg may activate immune cells, contributing to inflammation.
Area of Science:
- Biochemistry
- Immunology
- Nutritional Science
Background:
- Inflammatory processes are implicated in magnesium (Mg) deficiency pathology.
- The precise sequence of events initiating inflammation in Mg deficiency is not fully understood.
Purpose of the Study:
- To precisely characterize the acute phase response following Mg deficiency in rats.
- To investigate the early inflammatory events and immune cell activation in Mg-deficient rats.
Main Methods:
- Weaning male Wistar rats were fed Mg-deficient or control diets for 4 or 8 days.
- Analysis included leukocyte counts, subpopulations, plasma cytokine (IL-6) levels, acute phase proteins, fibrinogen, albumin, and liver mRNA expression.
- Peritoneal macrophages were assessed for activation and superoxide production.
Main Results:
- Mg-deficient rats exhibited an allergy-like crisis with altered leukocyte profiles and increased plasma IL-6 as early as day 4.
- Elevated plasma levels of acute phase proteins (alpha2-macroglobulin, alpha1-acid glycoprotein) and increased liver mRNA for these proteins were observed.
- Activated macrophages with enhanced superoxide production capacity were found in Mg-deficient rats, alongside increased fibrinogen and decreased albumin.
Conclusions:
- Inflammatory response is an early consequence of Mg deficiency in rats.
- Reduced extracellular Mg may directly contribute to the activated state of immune cells.
- Interleukin-6 appears to be an early indicator of inflammation in Mg deficiency, independent of Substance P.