Preventive Effect of Vitamin C on Dextran Sulfate Sodium (DSS)-Induced Colitis via the Regulation of IL-22 and IL-6 Production in Gulo(-/-) Mice.
Level 5 - mechanism / opinion, no new human data
Preclinical animal model study
PubMed 36142515 · doi:10.3390/ijms231810612
What was done
Researchers evaluated the impact of vitamin C status on experimental colitis using Gulo(-/-) mice, which cannot synthesize endogenous vitamin C due to a genetic disruption in L-gulono-γ-lactone oxidase. The authors compared vitamin C-insufficient Gulo(-/-) mice against vitamin C-sufficient Gulo(-/-) mice and wild-type controls, examining colon oxidative stress, mucosal integrity, immune cell infiltration, cytokine profiles (including IL-22 and IL-6), and associated signaling pathways (p38MAPK, STAT3, Akt).
What was found
The abstract reports qualitative directions without numerical values or effect sizes. Vitamin C-insufficient Gulo(-/-) mice showed extensive colon oxidative stress and increased inflammation. They also demonstrated decreased IL-22 production, reduced NKp46(+) cell recruitment, and impaired p38MAPK pathway activation. Furthermore, compared to vitamin C-sufficient Gulo(-/-) and wild-type mice, the insufficient mice had lower mucin-1 expression, higher IL-6 production, and increased activation of the STAT3 and Akt signaling cascades.
Why it matters
These findings suggest that dietary vitamin C plays a protective role in maintaining mucosal barrier integrity and regulating key inflammatory signaling cascades in models of colitis.
Limits
The study was conducted entirely in a genetically modified mouse model of chemically induced colitis, which does not capture the full complexity of human inflammatory bowel disease. The abstract does not provide sample sizes, vitamin C dosing regimens, quantitative data, or measures of variance.
Cited by
- supports In vitamin C-deficient mice with elevated pro-inflammatory cytokines, vitamin C administration normalizes cytokine production.