The DOI matches its Crossref record; 51 of the 51 references it cites were found in a registry or an index.
NLRP12 attenuates colon inflammation by maintaining colonic microbial diversity and promoting protective commensal bacterial growth
Open accessAbstract
Inflammatory bowel diseases involve the dynamic interaction of host genetics, the microbiome and inflammatory responses. Here we found lower expression of NLRP12 (which encodes a negative regulator of innate immunity) in human ulcerative colitis, by comparing monozygotic twins and other patient cohorts. In parallel, Nlrp12 deficiency in mice caused increased basal colonic inflammation, which led to a less-diverse microbiome and loss of protective gut commensal strains (of the family Lachnospiraceae) and a greater abundance of colitogenic strains (of the family Erysipelotrichaceae). Dysbiosis and susceptibility to colitis associated with Nlrp12 deficency were reversed equally by treatment with antibodies targeting inflammatory cytokines and by the administration of beneficial commensal Lachnospiraceae isolates. Fecal transplants from mice reared in specific-pathogen-free conditions into germ-free Nlrp12-deficient mice showed that NLRP12 and the microbiome each contributed to immunological signaling that culminated in colon inflammation. These findings reveal a feed-forward loop in which NLRP12 promotes specific commensals that can reverse gut inflammation, while cytokine blockade during NLRP12 deficiency can reverse dysbiosis.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Interestingly, two previous studies have indicated that changes in the relative abundance of gut microbiota are more likely to be influenced by inflammation rather than age, with TNF playing a significant role.185,186”
From Inflammation and aging: signaling pathways and intervention therapies (2023) · cites this paper as [185]
Experimental — accuracy not yet measured
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Naive Bayesian Classifier for Rapid Assignment of rRNA Sequences into the New Bacterial Taxonomy
Wang, Q., Garrity, G. M., Tiedje, J. M., & Cole, J. R. (2007) · Applied and Environmental Microbiology · doi:10.1128/aem.00062-07 · Cited by 20,145
Association of NOD2 leucine-rich repeat variants with susceptibility to Crohn's disease
Hugot, J.-P., Chamaillard, M., Zouali, H., Lesage, S., Cézard, J.-P., Belaiche, J., Almer, S., Tysk, C., O'Morain, C. A., Gassull, M., et al. (2001) · Nature · doi:10.1038/35079107 · Cited by 5,591
The Microbial Metabolites, Short-Chain Fatty Acids, Regulate Colonic T reg Cell Homeostasis
Smith, P. M., Howitt, M. R., Panikov, N., Michaud, M., Gallini, C. A., Bohlooly-Y, M., Glickman, J. N., & Garrett, W. S. (2013) · Science · doi:10.1126/science.1241165 · Cited by 5,413
A frameshift mutation in NOD2 associated with susceptibility to Crohn's disease
Ogura, Y., Bonen, D. K., Inohara, N., Nicolae, D. L., Chen, F. F., Ramos, R., Britton, H., Moran, T., Karaliuskas, R., Duerr, R. H., et al. (2001) · Nature · doi:10.1038/35079114 · Cited by 5,030
Metabolites produced by commensal bacteria promote peripheral regulatory T-cell generation
Arpaia, N., Campbell, C., Fan, X., Dikiy, S., van der Veeken, J., deRoos, P., Liu, H., Cross, J. R., Pfeffer, K., Coffer, P. J., et al. (2013) · Nature · doi:10.1038/nature12726 · Cited by 4,838
Richness of human gut microbiome correlates with metabolic markers
Le Chatelier, E., Nielsen, T., Qin, J., Prifti, E., Hildebrand, F., Falony, G., Almeida, M., Arumugam, M., Batto, J.-M., Kennedy, S., et al. (2013) · Nature · doi:10.1038/nature12506 · Cited by 4,662
Frank, D. N., St. Amand, A. L., Feldman, R. A., Boedeker, E. C., Harpaz, N., & Pace, N. R. (2007) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0706625104 · Cited by 4,611
Gut Microbiota from Twins Discordant for Obesity Modulate Metabolism in Mice
Ridaura, V. K., Faith, J. J., Rey, F. E., Cheng, J., Duncan, A. E., Kau, A. L., Griffin, N. W., Lombard, V., Henrissat, B., Bain, J. R., et al. (2013) · Science · doi:10.1126/science.1241214 · Cited by 3,788
The Treatment-Naive Microbiome in New-Onset Crohn’s Disease
Gevers, D., Kugathasan, S., Denson, L. A., Vázquez-Baeza, Y., Van Treuren, W., Ren, B., Schwager, E., Knights, D., Song, S. J., Yassour, M., et al. (2014) · Cell Host & Microbe · doi:10.1016/j.chom.2014.02.005 · Cited by 3,220
Human nutrition, the gut microbiome and the immune system
Kau, A. L., Ahern, P. P., Griffin, N. W., Goodman, A. L., & Gordon, J. I. (2011) · Nature · doi:10.1038/nature10213 · Cited by 2,588
Cited by
Sorted by citations
Inflammation and aging: signaling pathways and intervention therapies
Li, X., Li, C., Zhang, W., Wang, Y., Qian, P., & Huang, H. (2023) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-023-01502-8 · Cited by 1,443
“Interestingly, two previous studies have indicated that changes in the relative abundance of gut microbiota are more likely to be influenced by inflammation rather than age, with TNF playing a significant role.(185,186) This suggests that the changes in gut microbiota are more closely related with inflammatory process…”
ResultInflammasome activation and regulation: toward a better understanding of complex mechanisms
Zheng, D., Liwinski, T., & Elinav, E. (2020) · Cell Discovery · doi:10.1038/s41421-020-0167-x · Cited by 1,078
Gut Microbiota as a Trigger for Metabolic Inflammation in Obesity and Type 2 Diabetes
Scheithauer, T. P. M., Rampanelli, E., Nieuwdorp, M., Vallance, B. A., Verchere, C. B., van Raalte, D. H., & Herrema, H. (2020) · Frontiers in Immunology · doi:10.3389/fimmu.2020.571731 · Cited by 715
“It has been shown to dampen and resolve inflammation, in particular in the intestine, in a microbiota dependent manner (228) and by promoting the growth of beneficial bacteria (228).”
BackgroundDiverging inflammasome signals in tumorigenesis and potential targeting
Karki, R., & Kanneganti, T. (2019) · Nature reviews. Cancer · doi:10.1038/s41568-019-0123-y · Cited by 648
Multi-omics analyses of radiation survivors identify radioprotective microbes and metabolites
Guo, H., Chou, W.-C., Lai, Y., Liang, K., Tam, J. W., Brickey, W. J., Chen, L., Montgomery, N. D., Li, X., Bohannon, L. M., et al. (2020) · Science · doi:10.1126/science.aay9097 · Cited by 561
Self-citation
Metadata
- Authors
- Chen, L., Wilson, J. E., Koenigsknecht, M. J., Chou, W.-C., Montgomery, S. A., Truax, A. D., Brickey, W. J., Packey, C. D., Maharshak, N., Matsushima, G. K., Plevy, S. E., Young, V. B., Sartor, R. B., & Ting, J. P.-Y.
- Affiliations
- University of North Carolina at Chapel Hill (US)
- University of Michigan (US)
- Columbia University Irving Medical Center (US)
- Tel Aviv University (IL)
- Janssen (United States) (US)
- Corresponding author
- Ting, Jenny P-Y
- ORCID
- Venue
- Nature Immunology
- Published
- 2017-03-13
- Volume
- 18
- Issue
- 5
- Pages
- 541-551
- ISSN
- 1529-2908 (ISSN-L)
- 1529-2916
- PMC
- PMC5395345
- OpenAlex
- W2596103622
- Cited by
- 310
- References
- 51
- Citations by year
- 2026: 18 · 2025: 32 · 2024: 35 · 2023: 34 · 2022: 32 · 2021: 30 · 2020: 39 · 2019: 42 · 2018: 31 · 2017: 16
- FWCI
- 14.30
- Type
- journal article
- Language
- en
- Update notices
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Nature Immunology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Carolina Digital Repository (University of North Carolina at Chapel Hill) (submittedVersion)
- UNC Libraries
- Funders
- Crohn's and Colitis Foundation of America (P30 DK034987)
- North Carolina State University (P30 DK034987)
- Crohn's and Colitis Foundation
- Multiple Sclerosis Society
- National Institutes of Health (DK034987, DK094779, AI029564, AI067798, P40OD010995)
- National Cancer Institute (R01CA156330, P30CA016086)
- National Institute of Allergy and Infectious Diseases (U19AI090871, R37AI029564, AI-067798, U19AI067798)
- National Institute of Diabetes and Digestive and Kidney Diseases (DK094779, F32DK098916, AI067798, P01DK094779, DK 034987, F32DK088417, P30DK034987)
- Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill
- Center for Gastrointestinal Biology and Disease, School of Medicine, University of North Carolina at Chapel Hill (P30 DK 034987)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
- Health Sciences › Medicine › Gastroenterology › Inflammatory Bowel Disease
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Keywords
- NLRP12, inflammatory bowel disease, ulcerative colitis, colonic inflammation, gut microbiota, microbial diversity, commensal bacteria, Lachnospiraceae, Erysipelotrichaceae, dysbiosis, innate immunity, cytokine inhibition, fecal microbiota transplantation, germ-free mice, monozygotic twins
- MeSH terms
- Clostridiales, Eubacteriales, Firmicutes, Bacillota, Animals, Colitis, Ulcerative, Colon, Feces, Humans, Immunity, Innate, Mice, Inbred C57BL, RNA, Ribosomal, 16S, Symbiosis, Twins, Monozygotic, Dextran Sulfate, Mice, Knockout, Biodiversity, Intracellular Signaling Peptides and Proteins, Mice, Gene-Environment Interaction, Microbiota
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review