| First Author | Waddell A | Year | 2021 |
| Journal | Sci Rep | Volume | 11 |
| Issue | 1 | Pages | 9575 |
| PubMed ID | 33953267 | Mgi Jnum | J:316337 |
| Mgi Id | MGI:6713039 | Doi | 10.1038/s41598-021-89119-1 |
| Citation | Waddell A, et al. (2021) IL-33 is produced by colon fibroblasts and differentially regulated in acute and chronic murine colitis. Sci Rep 11(1):9575 |
| abstractText | IL-33 is upregulated in ulcerative colitis and has a protective role in chemically-induced acute murine colitis. We aimed to determine whether IL-33 influences Il10(-/-) chronic colitis and its cellular source in health and during colitis. Il10(-/-)Il33(-/-) and Il10(-/-)Il33(+/+) littermates developed colitis of similar severity. Colon Il33 was induced in WT and Il10(-/-) mice exposed to DSS, but not in unchallenged Il10(-/-) mice with colitis. Il33-citrine reporter mice showed that Il33-citrine colocalized with alpha-smooth muscle actin(+) myofibroblasts and vimentin(+) fibroblasts in WT mice. Citrine(+)CD74(+)CD90(hi) inflammatory fibroblasts were increased with DSS treatment. IL-1beta induced Il33 expression in colon myofibroblasts, but colon Il33 expression did not differ between DSS-treated WT and Il1r1(-/-) mice. In conclusion, deficiency of IL-33 does not alter the severity of chronic colitis in Il10(-/-) mice. Induction of Il33 upon DSS exposure in WT and Il10(-/-) mice, but not in unchallenged Il10(-/-) mice, suggests epithelial injury induces colon IL-33. Fibroblasts are the primary colonic source of IL-33 and IL-33-expressing CD90(hi)CD74(+) fibroblasts are increased during DSS-induced colitis. IL-1beta induces Il33 in colon myofibroblasts in vitro, but signaling through the IL-1R1 is not necessary for induction of IL-33 in DSS-induced colitis. |
