A113 LINKING GENE-ENVIRONMENT INTERACTIONS IN IBD: VITAMIN D-MEDIATED REGULATION OF AUTOPHAGY
Bibliographic record
Abstract
The incidence of IBD has risen dramatically over the past decade, indicating a role for environmental factors in disease onset. Growing evidence from animal and human studies indicate that vitamin D deficiency is an important environmental factor contributing to IBD pathogenesis, although the exact mechanism involved remains unknown. Autophagy is a pathway that has gained interest for its recently established role in IBD pathogenesis. Previously in our lab, we have shown that inducing vitamin D deficiency in wildtype C57Bl/6 mice causes a significant downregulation of autophagy proteins ATG16L1 and LC3II in the intestine. We aim to elucidate the relationship between vitamin D deficiency and IBD by exploring the effect of vitamin D on intestinal autophagy. We hypothesize that vitamin D deficiency plays a role in the dysregulation of autophagy in the intestine. To complement our previous findings and to directly assess the effect of vitamin D on intestinal epithelial cells and autophagy, we employed in vitro experiments using murine intestinal epithelial (MODE-K) cells and murine intestinal organoids. Cells were incubated with increasing concentrations of the active form of vitamin D. Western blotting was performed to evaluate autophagy markers ATG16L1 and LC3II, as well as the vitamin D receptor (VDR), a vitamin D responsive gene. As expected, a significant and dose-dependent increase in VDR expression was detected in cells incubated with vitamin D. Furthermore, a trend towards increased ATG16L1 was detected in vitamin D treated cells. Our findings suggest that vitamin D upregulates the autophagy protein ATG16L1 providing a potential mechanism by which vitamin D deficiency modulates IBD pathogenesis. Given this interesting interaction between vitamin D and autophagy, the next step of this project is to assess the effect of vitamin D deficiency in the context of IBD susceptibility Nod2 mutations. CCCOGS, Restracomp
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How this classification was reachedexpand
Full frame machine prediction
Teacher imitationNot calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.
Distilled classifier scores by category (both heads)
| Category | Codex | Gemma |
|---|---|---|
| Metaresearch | 0.000 | 0.000 |
| Meta-epidemiology (narrow) | 0.000 | 0.000 |
| Meta-epidemiology (broad) | 0.000 | 0.001 |
| Bibliometrics | 0.001 | 0.000 |
| Science and technology studies | 0.000 | 0.000 |
| Scholarly communication | 0.001 | 0.000 |
| Open science | 0.000 | 0.000 |
| Research integrity | 0.001 | 0.001 |
| Insufficient payload (model declined to judge) | 0.004 | 0.000 |
Machine scores (provisional)
The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.
Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.
score_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from itClassification
machine, unvalidatedMachine predicted; a candidate call from one source (direct Gemma or distilled Codex), not a consensus.
How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".