Publications by authors named "Wan-Jung H Wu"

Article Synopsis
  • Chronic high-fat diets (HFD) worsen intestinal diseases and cause sustained tissue damage by accumulating dead neutrophils and dietary lipids.
  • Depleting neutrophils can improve intestinal damage, while macrophages from HFD-fed mice struggle to clear dead neutrophils due to lipid interference.
  • The study shows that this interference impairs production of IL-10, a key molecule for healing, suggesting that HFD contributes to ongoing intestinal damage by disrupting macrophage function.
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The gut microbiota is essential for maintenance and repair of the intestinal epithelial barrier. As shifts in both intestinal epithelial barrier function and microbiota composition are found in inflammatory bowel disease patients, it is critical to understand the role of distinct bacteria in regulating barrier repair. We identified a mouse commensal isolate, GDAR2-2, that protects mice from infection and dextran sulfate sodium-induced colitis.

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Humans and their microbiota have coevolved a mutually beneficial relationship in which the human host provides a hospitable environment for the microorganisms and the microbiota provides many advantages for the host, including nutritional benefits and protection from pathogen infection. Maintaining this relationship requires a careful immune balance to contain commensal microorganisms within the lumen while limiting inflammatory anti-commensal responses. Antigen-specific recognition of intestinal microorganisms by T cells has previously been described.

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Autoimmune diseases and chronic inflammatory disorders are characterized by dysregulated immune responses resulting in excessive and uncontrolled tissue inflammation. Multiple factors including genetic variation, environmental stimuli, and infection are all thought to contribute to continued inflammation and pathology. Current evidence supports the microbiota as one such factor with emerging data linking commensal organisms to the onset and progression of disease.

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