Insights into the pathophysiology of ulcerative colitis: interleukin-13 modulates STAT6 and p38 MAPK activity in the colon epithelial sodium channel
| Autor: | Katharine A. Bresnahan, Peter R. Wiedmeier, T. Gardner, Shelby M. Quarnberg, Ian A. Sroufe |
|---|---|
| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
Epithelial sodium channel Molecular and cellular Colon Physiology p38 mitogen-activated protein kinases p38 Mitogen-Activated Protein Kinases 03 medical and health sciences Intestinal mucosa medicine Humans Intestinal Mucosa Colitis Epithelial Sodium Channels STAT6 Interleukin-13 business.industry medicine.disease Ulcerative colitis Pathophysiology 030104 developmental biology Interleukin 13 Cancer research Colitis Ulcerative STAT6 Transcription Factor business |
| Zdroj: | The Journal of Physiology. 595:421-422 |
| ISSN: | 0022-3751 |
| DOI: | 10.1113/jp272492 |
| Popis: | Interleukin‐13 (IL‐13) causes intestinal epithelial barrier dysfunction, and is implicated in the pathogenesis of Th2‐driven intestinal inflammation (e.g. ulcerative colitis). However, it is unclear whether the epithelial sodium channel (ENaC) – the main limiting factor for sodium absorption in the distal colon – is also influenced by IL‐13 and if so, by what mechanism(s).We demonstrate in an intestinal cell model as well as in mouse distal colon that IL‐13 causes reduced ENaC activity.We show that IL‐13 impairs ENaC‐dependent sodium transport by activating the JAK1/2–STAT6 signalling pathway.These results improve our understanding of the mechanisms through which IL‐13 functions as a key effector cytokine in ulcerative colitis, thereby contributing to the distinct pathology of this disease. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
Plný text