Dietary magnesium alleviates experimental murine colitis through upregulation of the transient receptor potential melastatin 6 channel

Valentina Trapani, Valentina Petito, Angelica Di Agostini, Daniela Arduini, Willem Hamersma, Giuseppe Pietropaolo, Francesca Luongo, Vincenzo Arena, Egidio Stigliano, Loris R. Lopetuso, Antonio Gasbarrini, Federica I. Wolf, Franco Scaldaferri

Research output: Contribution to journalArticle

Abstract

Background: Magnesium (Mg) is essential for human health and is absorbed mainly in the intestine. In view of the likely occurrence of an Mg deficit in inflammatory bowel disease (IBD) and the documented role of Mg in modulating inflammation, the present study addresses whether Mg availability can affect the onset and progression of intestinal inflammation. Methods: To study the correlation between Mg status and disease activity, we measured magnesemia by atomic absorption spectroscopy in a cohort of IBD patients. The effects of dietary Mg modulation were assessed in a murine model of dextran sodium sulfate (DSS)-induced colitis by monitoring magnesemia, weight, fecal occult blood, diarrhea, colon length, and histology. Expression of the transient receptor potential melastatin (TRPM) 6 channel was assessed by real-time reverse transcription polymerase chain reaction and immunohistochemistry in murine colon tissues. The effect of Mg on epithelial barrier formation/repair was evaluated in human colon cell lines. Results: Inflammatory bowel disease patients presented with a substantial Mg deficit, and serum Mg levels were inversely correlated with disease activity. In mice, an Mg-deficient diet caused hypomagnesemia and aggravated DSS-induced colitis. Colitis severely compromised intestinal Mg2+ absorption due to mucosal damage and reduction in TRPM6 expression, but Mg supplementation resulted in better restoration of mucosal integrity and channel expression. Conclusions: Our results highlight the importance of evaluating and correcting magnesemia in IBD patients. The murine model suggests that Mg supplementation may represent a safe and cost-effective strategy to reduce inflammation and restore normal mucosal function.

Original languageEnglish
Pages (from-to)2198-2210
Number of pages13
JournalInflammatory Bowel Diseases
Volume24
Issue number10
DOIs
Publication statusPublished - Oct 1 2018

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Colitis
Magnesium
Up-Regulation
Inflammatory Bowel Diseases
Dextran Sulfate
Colon
Inflammation
Occult Blood
Intestinal Absorption
Reverse Transcription
Intestines
Diarrhea
Spectrum Analysis
Histology
Immunohistochemistry
Diet
Weights and Measures
Costs and Cost Analysis
Cell Line

Keywords

  • Colon
  • Dextran sodium sulfate
  • Hypomagnesemia
  • Inflammatory bowel disease
  • Tumor necrosis factor-α

ASJC Scopus subject areas

  • Immunology and Allergy
  • Gastroenterology

Cite this

Dietary magnesium alleviates experimental murine colitis through upregulation of the transient receptor potential melastatin 6 channel. / Trapani, Valentina; Petito, Valentina; Di Agostini, Angelica; Arduini, Daniela; Hamersma, Willem; Pietropaolo, Giuseppe; Luongo, Francesca; Arena, Vincenzo; Stigliano, Egidio; Lopetuso, Loris R.; Gasbarrini, Antonio; Wolf, Federica I.; Scaldaferri, Franco.

In: Inflammatory Bowel Diseases, Vol. 24, No. 10, 01.10.2018, p. 2198-2210.

Research output: Contribution to journalArticle

Trapani, V, Petito, V, Di Agostini, A, Arduini, D, Hamersma, W, Pietropaolo, G, Luongo, F, Arena, V, Stigliano, E, Lopetuso, LR, Gasbarrini, A, Wolf, FI & Scaldaferri, F 2018, 'Dietary magnesium alleviates experimental murine colitis through upregulation of the transient receptor potential melastatin 6 channel', Inflammatory Bowel Diseases, vol. 24, no. 10, pp. 2198-2210. https://doi.org/10.1093/ibd/izy186
Trapani, Valentina ; Petito, Valentina ; Di Agostini, Angelica ; Arduini, Daniela ; Hamersma, Willem ; Pietropaolo, Giuseppe ; Luongo, Francesca ; Arena, Vincenzo ; Stigliano, Egidio ; Lopetuso, Loris R. ; Gasbarrini, Antonio ; Wolf, Federica I. ; Scaldaferri, Franco. / Dietary magnesium alleviates experimental murine colitis through upregulation of the transient receptor potential melastatin 6 channel. In: Inflammatory Bowel Diseases. 2018 ; Vol. 24, No. 10. pp. 2198-2210.
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AU - Trapani, Valentina

AU - Petito, Valentina

AU - Di Agostini, Angelica

AU - Arduini, Daniela

AU - Hamersma, Willem

AU - Pietropaolo, Giuseppe

AU - Luongo, Francesca

AU - Arena, Vincenzo

AU - Stigliano, Egidio

AU - Lopetuso, Loris R.

AU - Gasbarrini, Antonio

AU - Wolf, Federica I.

AU - Scaldaferri, Franco

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N2 - Background: Magnesium (Mg) is essential for human health and is absorbed mainly in the intestine. In view of the likely occurrence of an Mg deficit in inflammatory bowel disease (IBD) and the documented role of Mg in modulating inflammation, the present study addresses whether Mg availability can affect the onset and progression of intestinal inflammation. Methods: To study the correlation between Mg status and disease activity, we measured magnesemia by atomic absorption spectroscopy in a cohort of IBD patients. The effects of dietary Mg modulation were assessed in a murine model of dextran sodium sulfate (DSS)-induced colitis by monitoring magnesemia, weight, fecal occult blood, diarrhea, colon length, and histology. Expression of the transient receptor potential melastatin (TRPM) 6 channel was assessed by real-time reverse transcription polymerase chain reaction and immunohistochemistry in murine colon tissues. The effect of Mg on epithelial barrier formation/repair was evaluated in human colon cell lines. Results: Inflammatory bowel disease patients presented with a substantial Mg deficit, and serum Mg levels were inversely correlated with disease activity. In mice, an Mg-deficient diet caused hypomagnesemia and aggravated DSS-induced colitis. Colitis severely compromised intestinal Mg2+ absorption due to mucosal damage and reduction in TRPM6 expression, but Mg supplementation resulted in better restoration of mucosal integrity and channel expression. Conclusions: Our results highlight the importance of evaluating and correcting magnesemia in IBD patients. The murine model suggests that Mg supplementation may represent a safe and cost-effective strategy to reduce inflammation and restore normal mucosal function.

AB - Background: Magnesium (Mg) is essential for human health and is absorbed mainly in the intestine. In view of the likely occurrence of an Mg deficit in inflammatory bowel disease (IBD) and the documented role of Mg in modulating inflammation, the present study addresses whether Mg availability can affect the onset and progression of intestinal inflammation. Methods: To study the correlation between Mg status and disease activity, we measured magnesemia by atomic absorption spectroscopy in a cohort of IBD patients. The effects of dietary Mg modulation were assessed in a murine model of dextran sodium sulfate (DSS)-induced colitis by monitoring magnesemia, weight, fecal occult blood, diarrhea, colon length, and histology. Expression of the transient receptor potential melastatin (TRPM) 6 channel was assessed by real-time reverse transcription polymerase chain reaction and immunohistochemistry in murine colon tissues. The effect of Mg on epithelial barrier formation/repair was evaluated in human colon cell lines. Results: Inflammatory bowel disease patients presented with a substantial Mg deficit, and serum Mg levels were inversely correlated with disease activity. In mice, an Mg-deficient diet caused hypomagnesemia and aggravated DSS-induced colitis. Colitis severely compromised intestinal Mg2+ absorption due to mucosal damage and reduction in TRPM6 expression, but Mg supplementation resulted in better restoration of mucosal integrity and channel expression. Conclusions: Our results highlight the importance of evaluating and correcting magnesemia in IBD patients. The murine model suggests that Mg supplementation may represent a safe and cost-effective strategy to reduce inflammation and restore normal mucosal function.

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