Evidence map›Paper›PMID 42020416›Full record

ArticleNature communications2026

Ketogenic diet exacerbates DSS-induced colitis through a β-hydroxybutyrate-Thomasclavelia spiroformis-γδ17 T cell axis in mice.

Yameng Liu, Xuan Wu, Li Chen, Shan Wang, Jingyi Xu, Weifeng Wang, Xueting Yao, Wei Xie, Xianchun Zhong, Shuai Li and 6 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Review
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

16 authors.

Yameng Liu *Department of Laboratory Medicine, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, P. R. China.
Xuan Wu *Department of Laboratory Medicine, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, P. R. China.
Li Chen *Department of Rheumatology and Autoimmunology, The First Affiliated Hospital of Shandong First Medical University & Shandong Provincial Qianfoshan Hospital, Shandong Provincial Lab for Clinical Immunology Translational Medicine in Universities, Jinan, Shandong, 250014, P. R. China.
Shan Wang *The International Cooperation Laboratory on Signal Transduction, National Center for Liver Cancer, Eastern Hepatobiliary Surgery Hospital, Naval Medical University, Shanghai, P. R. China.
Jingyi Xu *School of Chinese Materia Medica, Nanjing University of Chinese Medicine, Nanjing, Jiangsu, P. R. China.ORCID http://orcid.org/0009-0004-4534-5536
Weifeng WangDepartment of Laboratory Medicine, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, P. R. China.
Xueting YaoDepartment of Laboratory Medicine, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, P. R. China.
Wei XieState Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, P. R. China.
Xianchun ZhongState Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, P. R. China.
Shuai LiThe International Cooperation Laboratory on Signal Transduction, National Center for Liver Cancer, Eastern Hepatobiliary Surgery Hospital, Naval Medical University, Shanghai, P. R. China.
Yueying LiDepartment of Laboratory Medicine, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, P. R. China.
Lin HanCentral Laboratory and Department of Laboratory Medicine, Shanghai Tenth People's Hospital, Tongji University, Shanghai, P. R. China.
Cen XieState Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, P. R. China. xiecen@simm.ac.cn.ORCID http://orcid.org/0000-0002-4574-8456
Lei ChenThe International Cooperation Laboratory on Signal Transduction, National Center for Liver Cancer, Eastern Hepatobiliary Surgery Hospital, Naval Medical University, Shanghai, P. R. China. chenlei@smmu.edu.cn.ORCID http://orcid.org/0000-0002-9380-9559
Frank J GonzalezLaboratory of Metabolism, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA.ORCID http://orcid.org/0000-0002-7990-2140
Weiwei LiuDepartment of Laboratory Medicine, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, P. R. China. huashanvivian@126.com.ORCID http://orcid.org/0000-0001-5069-9727

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ketogenic diet (KD) is widely recognized for its immunomodulatory and metabolic benefits, but the impact on inflammatory bowel disease remains controversial. Here, we demonstrate that KD maintains homeostasis under physiological conditions but exacerbates colitis by triggering a ketogenesis-microbe-immune cascade upon mucosal injury. Mechanistically, KD elevates luminal β-hydroxybutyrate (β-HB), promoting the expansion of Thomasclavelia spiroformis (T. spiroformis). In turn, T. spiroformis activates colonic γδ17 T cells via cell wall components, ultimately driving IL-17A-mediated iinflammation. Adoptive transfer of γδ17 T cells into Tcrd

Indexed as

3-Hydroxybutyric AcidColitisDiet, KetogenicTh17 CellsAdoptive TransferAnimalsColitis, UlcerativeColonDextran SulfateDisease Models, AnimalFemaleHumansInterleukin-17Intestinal MucosaMaleMice3-Hydroxybutyric AcidDextran SulfateInterleukin-17

Identifiers

PMID42020416
PMCPMC13314964

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.