immune system
• mice with DSS-induced inflammatory bowel disease show increased infiltration of inflammatory cells
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• mice exhibit increased susceptibility to inflammatory bowel disease (IBD), with mice showing more pronounced weight loss, earlier bloody feces and higher feces album level, increased destruction of intestinal architecture and crypts loss, increased infiltration of inflammatory cells, obvious edema and reduction in colon length after dextran sodium sulfate (DSS) administration
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digestive/alimentary system
• mice show higher feces album level when treated with DSS to induce IBD
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• mice show increased destruction of intestinal architecture and crypt loss when treated with DSS to induce IBD
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• mice with DSS-induced IBD show a reduction in colon length
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• mice with DSS-induced IBD show obvious edema
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• ATP-induced intracellular calcium concentration is higher in intestinal organoids, indicating a calcium overload
• permeability of intestinal organoids is increased
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• mice show a slower regeneration of intestinal organoids than in wild-type mice, showing a smaller size and slowed differentiation
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• mice with DSS-induced inflammatory bowel disease show increased infiltration of inflammatory cells
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• mice exhibit increased susceptibility to inflammatory bowel disease (IBD), with mice showing more pronounced weight loss, earlier bloody feces and higher feces album level, increased destruction of intestinal architecture and crypts loss, increased infiltration of inflammatory cells, obvious edema and reduction in colon length after dextran sodium sulfate (DSS) administration
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growth/size/body
• mice show increased weight loss when treated with dextran sodium sulfate to induce IBD
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homeostasis/metabolism
• mice with DSS-induced IBD show obvious edema
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cellular
• reactive oxygen species (ROS) production is elevated in intestinal organoids
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