We found a match
Your institution may have access to this item. Find your institution then sign in to continue.
- Title
Aryl Hydrocarbon Receptor Regulates Muc2 Production Independently of IL-22 during Colitis.
- Authors
Saxena, Archana; Mitchell, Chandani; Bogdon, Raymond; Roark, Kasie; Wilson, Kiesha; Staley, Shanieka; Hailey, Michelle; Williams, Michal Claire; Rutkovsky, Alex; Nagarkatti, Prakash; Nagarkatti, Mitzi; Busbee, Philip Brandon
- Abstract
We previously reported that an aryl hydrocarbon receptor (AhR) ligand, indole-3-carbinol (I3C), was effective at reducing colitis severity through immune cell-mediated interleukin-22 (IL-22) production. Intestinal epithelial cells (IECs) are also involved in regulating colitis, so we investigated their AhR-mediated mechanisms in the current report. A transcriptome analysis of IECs in wildtype (WT) mice revealed that during colitis, I3C regulated select mucin proteins, which could be attributed to goblet cell development. To address this, experiments under in vivo colitis (mice) or in vitro colon organoid conditions were undertaken to determine how select mucin proteins were altered in the absence or presence of AhR in IECs during I3C treatment. Comparing WT to IEC-specific AhR knockout mice (AhRΔIEC), the results showed that AhR expression was essential in IECs for I3C-mediated protection during colitis. AhR-deficiency also impaired mucin protein expression, particularly mucin 2 (Muc2), independently of IL-22. Collectively, this report highlights the important role of AhR in direct regulation of Muc2. These results provide justification for future studies aimed at determining how AhR might regulate select mucins through mechanisms such as direct transcription binding to enhance production.
- Subjects
ARYL hydrocarbon receptors; COLITIS; KNOCKOUT mice; INTERLEUKIN-22; EPITHELIAL cells; PLANT protection
- Publication
International Journal of Molecular Sciences, 2024, Vol 25, Issue 4, p2404
- ISSN
1661-6596
- Publication type
Article
- DOI
10.3390/ijms25042404