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Analyzing Beneficial Effects of Nutritional Supplements on Intestinal Epithelial Barrier Functions During Experimental Colitis
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Dietary Salt Exacerbates Experimental Colitis.

Alan L Tubbs1,2,3, Bo Liu1,3, Troy D Rogers4

  • 1Center for Gastrointestinal Biology and Disease, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599.

Journal of Immunology (Baltimore, Md. : 1950)
|June 23, 2017
PubMed
Summary
This summary is machine-generated.

High salt intake exacerbates inflammatory bowel disease (IBD) pathology in mice by increasing proinflammatory cytokines. This suggests dietary salt may be an environmental factor driving IBD inflammation.

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Area of Science:

  • Gastroenterology
  • Immunology
  • Nutrition Science

Background:

  • The Western diet is linked to inflammatory bowel disease (IBD) but high salt content is understudied.
  • Processed foods, common in Western diets, are high in sodium chloride.

Purpose of the Study:

  • To investigate the role of high salt diets (HSD) as a potential environmental factor in IBD pathogenesis.
  • To examine the effects of HSD on inflammatory responses in murine colitis models.

Main Methods:

  • Murine models of colitis (IL-10-deficient and Salmonella typhimurium infection) were fed HSD or low salt diets.
  • Cytokine expression and immune cell responses were analyzed.
  • Dendritic cells were cultured in high salt media to assess activation pathways.

Main Results:

  • HSD exacerbated colitis pathology and increased proinflammatory cytokine expression in IL-10-deficient mice.
  • Sodium accumulated in the colons of mice on HSD.
  • HSD potentiated innate immune responses and cytokine expression during Salmonella infection.
  • High salt media enhanced cytokine production in dendritic cells via TLR4/p38 MAPK/SGK1 pathways.

Conclusions:

  • High dietary salt intake may be an environmental factor contributing to IBD inflammation.
  • HSD can exacerbate inflammatory responses and potentiate innate immunity, suggesting a direct role for salt in IBD pathogenesis.