Evidence map›Paper›PMID 25725098›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2015

The NLRP1 inflammasome attenuates colitis and colitis-associated tumorigenesis.

Tere M Williams, Rachel A Leeth, Daniel E Rothschild, Sheryl L Coutermarsh-Ott, Dylan K McDaniel, Alysha E Simmons, Bettina Heid, Thomas E Cecere, Irving C Allen

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 110 papers.

0numbers the graph read from it
0cells of the map it votes in
110citing papers in PubMed
6.8field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

110 citing papers in PubMed, 162 citations in OpenAlex.

  1. Review
  2. Review
  3. Pyroptosis: Turning Up the Heat on Cancer.Annual review of immunology · 2026
    Review
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  8. Article
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  18. Clinical signature and associated immune metabolism of NLRP1 in pan-cancer.Journal of cellular and molecular medicine · 2024
    Article
  19. Review
  20. Article

50 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 1 country.

Tere M WilliamsDepartment of Biomedical Sciences and Pathobiology, Virginia-Maryland College of Veterinary Medicine, Virginia Tech, Blacksburg, VA 24061.
Rachel A LeethDepartment of Biomedical Sciences and Pathobiology, Virginia-Maryland College of Veterinary Medicine, Virginia Tech, Blacksburg, VA 24061.
Daniel E RothschildDepartment of Biomedical Sciences and Pathobiology, Virginia-Maryland College of Veterinary Medicine, Virginia Tech, Blacksburg, VA 24061.
Sheryl L Coutermarsh-OttDepartment of Biomedical Sciences and Pathobiology, Virginia-Maryland College of Veterinary Medicine, Virginia Tech, Blacksburg, VA 24061.
Dylan K McDanielDepartment of Biomedical Sciences and Pathobiology, Virginia-Maryland College of Veterinary Medicine, Virginia Tech, Blacksburg, VA 24061.
Alysha E SimmonsDepartment of Biomedical Sciences and Pathobiology, Virginia-Maryland College of Veterinary Medicine, Virginia Tech, Blacksburg, VA 24061.
Bettina HeidDepartment of Biomedical Sciences and Pathobiology, Virginia-Maryland College of Veterinary Medicine, Virginia Tech, Blacksburg, VA 24061.
Thomas E CecereDepartment of Biomedical Sciences and Pathobiology, Virginia-Maryland College of Veterinary Medicine, Virginia Tech, Blacksburg, VA 24061.
Irving C AllenDepartment of Biomedical Sciences and Pathobiology, Virginia-Maryland College of Veterinary Medicine, Virginia Tech, Blacksburg, VA 24061 icallen@vt.edu.
Virginia Tech · USVirginia–Maryland College of Veterinary Medicine · US

Funding

VT Post Baccalaureate Research and Education ProgramR25GM066534 · NIGMS · VIRGINIA POLYTECHNIC INST AND ST UNIV · PI SMITH, EDWARD J · 2003 to 2024
$7.6M
VT Initiative for Maximizing Student DiversityR25GM072767 · NIGMS · VIRGINIA POLYTECHNIC INST AND ST UNIV · PI SMITH, EDWARD J · 2007 to 2021
$6.9M
NLR Regulation of Gastrointestinal Inflammation and TumorigenesisK01DK092355 · NIDDK · VIRGINIA POLYTECHNIC INST AND ST UNIV · PI ALLEN, IRVING C · 2011 to 2015
$709k
NIDDK NIH HHS K01 DK092355NIDDK NIH HHS K01DK092355NIGMS NIH HHS R25 GM066534NIGMS NIH HHS R25 GM072767
6 · The paper itself

Abstract

Nucleotide-binding domain and leucine-rich repeat (NLR) proteins are a diverse family of pattern recognition receptors that are essential mediators of inflammation and host defense in the gastrointestinal system. Recent studies have identified a subgroup of inflammasome forming NLRs that modulate the mucosal immune response during inflammatory bowel disease (IBD) and colitis associated tumorigenesis. To better elucidate the contribution of NLR family members in IBD and cancer, we conducted a retrospective analysis of gene expression metadata from human patients. These data revealed that NLRP1, an inflammasome forming NLR, was significantly dysregulated in IBD and colon cancer. To better characterize the function of NLRP1 in disease pathogenesis, we used Nlrp1b(-/-) mice in colitis and colitis-associated cancer models. In this paper, we report that NLRP1 attenuates gastrointestinal inflammation and tumorigenesis. Nlrp1b(-/-) mice demonstrated significant increases in morbidity, inflammation, and tumorigenesis compared with wild-type animals. Similar to data previously reported for related inflammasome forming NLRs, the increased inflammation and tumor burden was correlated with attenuated levels of IL-1β and IL-18. Further mechanistic studies using bone marrow reconstitution experiments revealed that the increased disease pathogenesis in the Nlrp1b(-/-) mice was associated with nonhematopoietic-derived cells and suggests that NLRP1 functions in the colon epithelial cell compartment to attenuate tumorigenesis. Taken together, these data identify NLRP1 as an essential mediator of the host immune response during IBD and cancer. These findings are consistent with a model whereby multiple NLR inflammasomes attenuate disease pathobiology through modulating IL-1β and IL-18 levels in the colon.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsApoptosis Regulatory ProteinsBiopsyCell Transformation, NeoplasticColitisColitis, UlcerativeColonic NeoplasmsDisease Models, AnimalDisease ProgressionGene ExpressionHumansInflammasomesInterleukin-18Interleukin-1betaMaleAdaptor Proteins, Signal TransducingApoptosis Regulatory ProteinsInflammasomesInterleukin-18Interleukin-1betaNLRP1 protein, humanNLR Proteins

Identifiers

PMID25725098
PMCPMC4369420
OpenAlexW1632263489

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.