title: Inflammatory response following acute magnesium deficiency in the rat.
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.
authors.affiliation: Centre de Recherches en Nutrition Humaine, Unité Maladies Métaboliques et Micronutriments, INRA, Theix, St. Genès Champanelle, France.
authors.forename: C
authors.initials: C
authors.lastname: Malpuech-Brugère
authors.forename: W
authors.initials: W
authors.lastname: Nowacki
authors.forename: M
authors.initials: M
authors.lastname: Daveau
authors.forename: E
authors.initials: E
authors.lastname: Gueux
authors.forename: C
authors.initials: C
authors.lastname: Linard
authors.forename: E
authors.initials: E
authors.lastname: Rock
authors.forename: J
authors.initials: J
authors.lastname: Lebreton
authors.forename: A
authors.initials: A
authors.lastname: Mazur
authors.forename: Y
authors.initials: Y
authors.lastname: Rayssiguier
mesh_terms: D000209:Acute-Phase Proteins / Q000378:metabolism; D000818:Animals; D000831:Animals, Newborn; D004032:Diet; D005340:Fibrinogen / Q000378:metabolism; D007249:Inflammation / Q000276:immunology*; D015850:Interleukin-6 / Q000097:blood; D007962:Leukocytes / Q000276:immunology / Q000378:metabolism; D008099:Liver / Q000378:metabolism; D008262:Macrophage Activation; D008275:Magnesium Deficiency / Q000276:immunology / Q000378:metabolism*; D008297:Male; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D012709:Serum Albumin / Q000378:metabolism; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D000209:Acute-Phase Proteins; D015850:Interleukin-6; D012333:RNA, Messenger; D012709:Serum Albumin; D014409:Tumor Necrosis Factor-alpha; D005340:Fibrinogen; D013755:Tetradecanoylphorbol Acetate