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Intestinal and cardiac inflammatory response shows enhanced endotoxin receptor (CD14) expression in magnesium
Joanna J Chmielinska1, M Isabel Tejero-Taldo, I Tong Mak
1Division of Experimental Medicine, Department of Biochemistry and Molecular Biology, USA. phyjch@gwumc.edu
Abstract:
Substance P is elevated in plasma and in other tissues during Mg-deficiency, and was found localised to neuronal C-fibres of cardiac and intestinal tissues, where it could promote neurogenic inflammation. Plasma prostaglandin E2 (PGE2), indicative of systemic inflammation, rose significantly (>or=4 fold, p<0.01) after 1 week and remained elevated through week 2 and 3 in rat on the Mg-deficient (MgD) diet. Concomitantly, total blood glutathione decreased by 50%. Immunohistochemical staining for endotoxin (lipopolysaccaride, LPS) receptor, CD14 was prominent in macrophage-type cells in intestinal tissue; more importantly, cardiac tissue revealed both CD11b (monocyte/macrophage surface protein) and CD14 positive cells after 3 weeks in rats on MgD diet. Western blot analysis indicated a significant increase in the endotoxin receptor protein level in the 3 week MgD hearts. Since CD14 is known to be up-regulated in cells exposed to LPS, these observations suggest that prolonged Mg-deficiency results in increased intestinal permeability to bacterial products that induce the endotoxin receptor in cells localized to myocardial and intestinal tissues. These CD14 positive cells may amplify the cardiomyopathic inflammatory process by stimulating TNF-alpha and other pro-inflammatory cytokines.
Insights
Magnesium deficiency elevates substance P and prostaglandin E2, indicating inflammation. This deficiency increases intestinal permeability to endotoxins, activating inflammatory pathways in heart and gut tissues.
Area of Science:
- Biochemistry
- Physiology
- Immunology
Background:
- Magnesium deficiency is linked to increased substance P and neurogenic inflammation.
- Systemic inflammation markers like prostaglandin E2 (PGE2) are elevated in magnesium-deficient rats.
- Glutathione levels decrease, suggesting increased oxidative stress.
Purpose of the Study:
- To investigate the role of magnesium deficiency in inflammation.
- To explore the link between magnesium deficiency, intestinal permeability, and endotoxin receptor expression.
- To examine the impact on cardiac and intestinal tissues.
Main Methods:
- Rats were fed a magnesium-deficient (MgD) diet.
- Plasma PGE2 and blood glutathione levels were measured.
- Immunohistochemistry was used to detect CD14 and CD11b expression in tissues.
- Western blot analysis quantified endotoxin receptor protein levels.
Main Results:
- MgD rats showed elevated plasma PGE2 and decreased blood glutathione.
- CD14 expression was prominent in intestinal macrophages and also detected in cardiac tissues.
- Cardiac tissue exhibited increased endotoxin receptor (CD14) protein levels after 3 weeks of MgD diet.
- These findings suggest increased intestinal permeability to lipopolysaccharide (LPS).
Conclusions:
- Prolonged magnesium deficiency increases intestinal permeability to bacterial products like LPS.
- This leads to upregulation of the endotoxin receptor CD14 in myocardial and intestinal tissues.
- CD14-positive cells may exacerbate cardiac inflammation by stimulating pro-inflammatory cytokines such as TNF-alpha.
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