Publications by authors named "M Kasaian"
Article Synopsis
- The study investigates how the chromatin and protein expressions of colonic epithelial cells differ between healthy individuals and patients with ulcerative colitis (UC), highlighting the role of epithelial dysfunction in UC pathology.
- Researchers sorted and analyzed epithelial cells from colon biopsies of healthy controls and UC patients to uncover these differences in proteome and chromatin accessibility.
- Results show significant protein elevation linked to inflammation in UC, with a notable reduction of the water channel aquaporin 8, indicating specific epigenetic mechanisms that influence protein expression in health vs. disease.
The intestinal epithelium comprises diverse cell types and executes many specialized functions as the primary interface between luminal contents and internal organs. A key function provided by the epithelium is maintenance of a barrier that protects the individual from pathogens, irritating luminal contents, and the microbiota. Disruption of this barrier can lead to inflammatory disease within the intestinal mucosa, and, in more severe cases, to sepsis.
View Article and Find Full Text PDFBackground: Patient-derived organoid (PDO) models offer potential to transform drug discovery for inflammatory bowel disease (IBD) but are limited by inconsistencies with differentiation and functional characterization. We profiled molecular and cellular features across a range of intestinal organoid models and examined differentiation and establishment of a functional epithelial barrier.
Methods: Patient-derived organoids or monolayers were generated from control or IBD patient-derived colon or ileum and were molecularly or functionally profiled.
IL-33 is a multifunctional cytokine that mediates local inflammation upon tissue damage. IL-33 is known to act on multiple cell types including group 2 innate lymphoid cells (ILC2s), Th2 cells, and mast cells to drive production of Th2 cytokines including IL-5 and IL-13. IL-33 signaling activity through transmembrane ST2L can be inhibited by soluble ST2 (sST2), which acts as a decoy receptor.
View Article and Find Full Text PDFThere continues to be a major need for more effective inflammatory bowel disease (IBD) therapies. IL-13Rα2 is a decoy receptor that binds the cytokine IL-13 with high affinity and diminishes its STAT6-mediated effector functions. Previously, we found that IL-13Rα2 was necessary for IBD in mice deficient in the anti-inflammatory cytokine IL-10.
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