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Record W2922017119 · doi:10.1093/jcag/gwz006.008

A9 IL37 SIGNALING THROUGH SIGIRR: A NOVEL APPROACH TO SUPPRESS INTESTINAL INFLAMMATION

2019· article· en· W2922017119 on OpenAlexaff
Joannie M. Allaire, Shauna M. Crowley, Xiurui Han, Art F. Y. Poon, Bruce A. Vallance

Bibliographic record

VenueJournal of the Canadian Association of Gastroenterology · 2019
Typearticle
Languageen
FieldMedicine
TopicDietary Effects on Health
Canadian institutionsBC Children's HospitalUniversity of British Columbia
Fundersnot available
KeywordsInflammationInnate immune systemImmunologyInnate lymphoid cellColitisInflammatory bowel diseaseReceptorCytokineBiologySignal transductionMedicineImmune systemDiseaseCell biologyInternal medicine

Abstract

fetched live from OpenAlex

Inflammatory bowel diseases (IBD) are chronic inflammatory diseases affecting 1 in every 150 Canadians. In contrast to healthy individuals, IBD patients develop exaggerated inflammatory responses against their resident microbiota, at the level of the single layer of epithelial cells (IEC) lining the intestinal tract. Typically, the innate immune hypo-responsiveness of IEC prevents such maladaptive responses, in part due to their strong expression of Single Ig IL-1 related receptor (SIGIRR), a negative regulator of interleukin (IL)-1 and toll-like receptor signaling. Its expression is reduced in IBD patients with active disease and in mouse models of colitis; its complete loss leads to necrotizing enterocolitis. Despite the importance of SIGIRR, its designation as an orphan receptor has limited its therapeutic potential to suppress inflammation. Recently however, IL-37, a newly recognized anti-inflammatory cytokine has been shown to signal through a receptor complex of SIGIRR and IL-18 receptor, to inhibit inflammatory signaling. Several studies have demonstrated that IL-37 inhibits innate signaling in cells expressing SIGIRR, thereby suppressing various forms of inflammation in mice. Study IL-37/SIGIRR effects on IEC innate signaling and infectious colitis. Using human IEC lines and human/mice derived intestinal organoids, we assessed the ability of IL37 to suppress innate signaling in IEC. IL37 transgenic mice and wildtype C57BL/6 mice injected with IL37 were used to define the in vivo effect of IL37 on gut inflammation during a bacterial (Salmonella typhimurium) driven colitis. Colitis severity was determined by macroscopic/histological scoring. qPCR, ELISA and Western blot measured cytokine, chemokine and antimicrobial peptide production; immunostaining quantified inflammatory cell recruitment. We found that IL-37 suppress innate immune signalling (NFkB activation; production of IL-8, CCL20 chemokine) in human IEC stimulated by bacteria and cytokines. Using organoids derived from wildtype and Sigirr-/- mice, we demonstrated that IL-37 suppress innate IEC responses (Il-6, Cxcl1 and TNFα mRNA transcription; NFkB activation) in a SIGIRR dependent manner. Using S. typhimuriuminfection, we showed that the responsiveness of wildtype mice to IL37 treatment protected them from S. typhimurium infection by reducing luminal and intracellular pathogen burdens, intestinal tissue pathology and inflammation in concert with reducing cytokine and chemokine secretion by IEC. Taken together, our studies show that IL37 offers potential to suppress intestinal inflammation, through it signal on SIGIRR expressing IEC. Further investigations will determine the ability of IL37 to control microbial dysbiosis, as the therapeutic potential of IL37/SIGIRR to promote gut health by suppressing IEC inflammatory/antimicrobial responses. CAG, CCC, CIHRMSFHR

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 score0.019
Threshold uncertainty score0.996

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 head0.015
GPT teacher head0.250
Teacher spread0.235 · 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
Published2019
Admission routes1
Has abstractyes

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