ArticleInflammatory bowel diseases2009
ROS, Hsp27, and IKKbeta mediate dextran sodium sulfate (DSS) activation of IkappaBa, NFkappaB, and IL-8.
Article in Inflammatory bowel diseases, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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34 citing papers in PubMed, 67 citations in OpenAlex.
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- Comparative Evaluation between Sulfasalazine Alone and in Combination with Herbal Medicine on DSS-Induced Ulcerative Colitis Mice.BioMed research international · 2017Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
backgroundDextran sodium sulfate (DSS) is a sulfated polysaccharide that has been very widely used to induce inflammation in experimental models of inflammatory bowel disease in which the effects of pharmacologic and biologic therapies are tested. However, the precise mechanisms by which DSS induces inflammation have not been elucidated.
methodsDSS-induced increases in phospho-IkappaBalpha, nuclear NFkappaB (p65), and IL-8 secretion in human colonic epithelial cells in tissue culture are attributable to a reactive oxygen species (ROS)-induced pathway of inflammation, and do not require TLR4, MyD88, or Bcl10, which are associated with the innate immune pathway of NFkappaB-IL-8 activation.
resultsDSS-induced increases were inhibited by the ROS scavengers Tempol and Tiron, were associated with decreased phosphorylation of MAPK12 (p38gamma), MAPK 13 (p38delta), and Hsp27, and required the IkappaB kinase (IKK) signalosome component IKKbeta. In ex vivo colonic tissue from TLR4-deficient mice, or following knockdown of MyD88 or Bcl10 or exposure to an IRAK 1/4 inhibitor, DSS effects were not suppressed. Data demonstrated that DSS activates IkappaBalpha, NFkappaB, and IL-8 through an ROS-Hsp27-IKKbeta-mediated pathway, and not through an innate immune cascade.
conclusionsThese results suggest that DSS models of inflammation may not be optimal for evaluation of interventions that involve mechanisms of innate immunity.
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