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Record W2789479325 · doi:10.1093/jcag/gwy009.088

A88 NLRP3 DRIVES INTESTINAL INFLAMMATION-ASSOCIATED FIBROSIS

2018· article· en· W2789479325 on OpenAlexaff
Jessica Tjong, Y Li, Justin A. MacDonald, Daniel A. Muruve, Paul L. Beck

Bibliographic record

VenueJournal of the Canadian Association of Gastroenterology · 2018
Typearticle
Languageen
FieldBiochemistry, Genetics and Molecular Biology
TopicDigestive system and related health
Canadian institutionsUniversity of Calgary
Fundersnot available
KeywordsCTGFFibrosisMyofibroblastInflammationInflammatory bowel diseaseConnective tissueMedicineWestern blotColitisImmunologyCancer researchPathologyReceptorBiologyInternal medicineGrowth factorBiochemistryDisease

Abstract

fetched live from OpenAlex

Fibrosis is one of the most common causes of surgery in inflammatory bowel disease (IBD) and the mechanisms of fibrosis in IBD are not well understood. Nucleotide-binding oligomerization domain (NOD)- like receptors, including NLRP3, are cytosolic protein sensors involved in inflammatory pathways and implicated in IBD pathogenesis. We have shown NLRP3 drives fibrosis in the heart and kidney; however, its role in intestinal fibrosis is unknown. We hypothesize that NLRP3 drives inflammation associated with intestinal fibrosis. 1) To determine, in vitro, if intestinal fibroblasts lacking NLRP3 are phenotypically distinct from wild type fibroblasts. 2) To assess intestinal fibrosis of NLRP3-deficient and wild type mice in a model of chronic colitis. 3) To investigate intestinal NLR expression in IBD patients and healthy controls. Primary colonic myofibroblasts were isolated from wild-type (WT) and Nlrp3-/- mice. Cells were treated with pro-fibrogenic cytokine TGF-beta and downstream signalling was assessed by western blot. To investigate the role of NLRP3 in intestinal fibrosis in vivo, WT and Nlrp3-/- mice were given 3 cycles of low percent (w/v) dextran sulfate sodium (DSS) in water for 5 days, followed by a two-week recovery period. In addition, we investigated the expression of NLRP3 transcripts in patients with IBD by qPCR of cDNA from mucosal biopsies. TGF-beta signalling is attenuated in Nlrp3-/- colonic myofibroblasts as phosphorylation of Smad2, a downstream TGF-beta signalling protein, was reduced in Nlrp3-/- myofibroblasts compared to WT. Nlrp3-/- myofibroblasts also had lower TGF-beta-induced connective tissue growth factor (CTGF) compared to WT. Nlrp3-/- mice are more susceptible to cyclical DSS treatment with significantly greater weight loss and mortality compared to WT. Marked intestinal fibrosis was induced with the cyclical DSS protocol and those with most severe fibrosis were Nlpr3-/- mice. NLRP3 transcript levels were significantly increased in Crohn’s Disease (CD) patients compared to normal controls, but not in ulcerative colitis (UC) patients. Our data suggest that loss of NLRP3 leads to reduced response to TGF-beta in colonic myofibroblasts. Similar to its role in the kidney and heart, NLRP3 may potentiate TGF-beta signalling in the gut. Further insights into the mechanisms of intestinal fibrosis will significantly impact the development of new tools that will help with assessing and treating patients with IBD complications. CIHR

Fetched live from OpenAlex and de-inverted. Abstracts are not stored in this database: the inverted indexes are 8.6 GB of the frame’s 9.3 GB of text, and the host has 13 GB free.

How this classification was reachedexpand

Full frame distilled prediction

Teacher imitation

Not calibrated prevalence, not ground truth. Human validation pending. Learned from the 10,348 direct Codex labels and 10,348 direct Gemma labels. Candidate is the union of thresholded teacher heads; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels or direct frontier model labels.

metaresearch head score (Codex)0.001
metaresearch head score (Gemma)0.001
Version: codex-gemma-dda1882f352aValidation status: machine_predicted_unvalidated
Candidate categoriesnone
Consensus categoriesnone
DomainCandidate signal: none · Consensus signal: none
Study designCandidate signal: Observational · Consensus signal: Observational
GenreCandidate signal: Empirical · Consensus signal: Empirical
Teacher disagreement score0.223
Threshold uncertainty score0.789

Codex and Gemma teacher scores by category

CategoryCodexGemma
Metaresearch0.0010.001
Meta-epidemiology (narrow)0.0000.000
Meta-epidemiology (broad)0.0000.000
Bibliometrics0.0000.000
Science and technology studies0.0000.000
Scholarly communication0.0000.000
Open science0.0000.000
Research integrity0.0000.000
Insufficient payload (model declined to judge)0.0000.000

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.

Opus teacher head0.005
GPT teacher head0.222
Teacher spread0.217 · how far apart the two teachers sit on this one work
Validation statusscore_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from it

Classification

machine, unvalidated

Machine predicted; a candidate call from one teacher head, not a consensus.

The models applied no category: nothing in the taxonomy fit this work.
Study designObservational
Domainnot available
GenreEmpirical

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".

Quick stats

Citations0
Published2018
Admission routes1
Has abstractyes

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