Evidence map›Paper›PMID 38062857›Full record

ArticleGut microbes2023

Gut microbiota-derived 12-ketolithocholic acid suppresses the IL-17A secretion from colonic group 3 innate lymphoid cells to prevent the acute exacerbation of ulcerative colitis.

Na Li, Peiguang Ma, Yalan Li, Xuekai Shang, Xinmei Nan, Lei Shi, Xiao Han, Jiajing Liu, Yanfei Hong, Qiuyi Li and 3 more

Open access · goldAbstract read
In one paragraph

Article in Gut microbes, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
7.6field-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

37 citing papers in PubMed, 46 citations in OpenAlex.

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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

13 authors at 1 institution in 1 country.

Na LiDepartment of Immunology and Microbiology, School of Life Sciences, Beijing University of Chinese Medicine, Beijing, People's Republic of China.
Peiguang MaDepartment of Immunology and Microbiology, School of Life Sciences, Beijing University of Chinese Medicine, Beijing, People's Republic of China.
Yalan LiDepartment of Immunology and Microbiology, School of Life Sciences, Beijing University of Chinese Medicine, Beijing, People's Republic of China.
Xuekai ShangDepartment of Immunology and Microbiology, School of Life Sciences, Beijing University of Chinese Medicine, Beijing, People's Republic of China.
Xinmei NanDepartment of Immunology and Microbiology, School of Life Sciences, Beijing University of Chinese Medicine, Beijing, People's Republic of China.
Lei ShiDepartment of Gastroenterology, Dong Fang Hospital, Beijing University of Chinese Medicine, Beijing, People's Republic of China.
Xiao HanDepartment of Gastroenterology, Dong Fang Hospital, Beijing University of Chinese Medicine, Beijing, People's Republic of China.
Jiajing LiuDepartment of Immunology and Microbiology, School of Life Sciences, Beijing University of Chinese Medicine, Beijing, People's Republic of China.
Yanfei HongDepartment of Immunology and Microbiology, School of Life Sciences, Beijing University of Chinese Medicine, Beijing, People's Republic of China.
Qiuyi LiDepartment of Immunology and Microbiology, School of Life Sciences, Beijing University of Chinese Medicine, Beijing, People's Republic of China.
Jiaqi CuiDepartment of Immunology and Microbiology, School of Life Sciences, Beijing University of Chinese Medicine, Beijing, People's Republic of China.
Junxiang LiDepartment of Gastroenterology, Dong Fang Hospital, Beijing University of Chinese Medicine, Beijing, People's Republic of China.
Guiying PengDepartment of Immunology and Microbiology, School of Life Sciences, Beijing University of Chinese Medicine, Beijing, People's Republic of China.ORCID 0000-0002-0358-2515
Beijing University of Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Intestinal microbiota dysbiosis and metabolic disruption are well-known as the primary triggers of ulcerative colitis (UC). However, their role in regulating the group 3 innate lymphoid cells (ILC3s), which are essential for intestinal health, remains unexplored during the development of disease severity. Here, our results showed that the microbiota structure of patients with severe UC (SUCs) differed from those with mild UC (MiUCs), moderate UC (MoUCs), and healthy controls (HCs). Microbes producing secondary bile acids (SBAs) and SBAs decreased with the aggravation of UC, and a strong positive correlation existed between them. Next, fecal microbiota transfer was used to reproduce the human-derived microbiota in mice and decipher the microbiota-mediated inflammatory modulation during an increase in disease severity. Mice receiving SUC-derived microbiota exhibited enhancive inflammation, a lowered percentage of ILC3s, and the down-regulated expressions of bile acid receptors, including vitamin D receptor (VDR) and pregnane X receptor (PXR), in the colon. Similar to clinical results, SBA-producing microbes, deoxycholic acids (DCA), and 12-ketolithocholic acids (12-KLCA) were diminished in the intestine of these recipients. Finally, we compared the therapeutic potential of DCA and 12-KLCA in preventing colitis and the regulatory mechanisms mediated by ILC3s. 12-KLCA but not DCA represented a strong anti-inflammatory effect associated with the higher expression of VDR and the lower secretion of IL-17A from colonic ILC3s. Collectively, these findings provide new signatures for monitoring the acute deterioration of UC by targeting gut microbiota and bile acid metabolism and demonstrate the therapeutic and preventive potential of a novel microbiota-derived metabolite, 12-KLCA.

Indexed as

ColitisColitis, UlcerativeGastrointestinal MicrobiomeAnimalsBile Acids and SaltsColonDextran SulfateDisease Models, AnimalHumansImmunity, InnateInterleukin-17Lithocholic AcidLymphocytesMiceMice, Inbred C57BL12-ketolithocholic acidBile Acids and SaltsDextran SulfateInterleukin-17Lithocholic Acidgroup 3 innate lymphoid cellsgut microbiotasecondary bile acidsUlcerative colitis

Identifiers

PMID38062857
PMCPMC10730201
OpenAlexW4389482700

What OpenQuestion holds

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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.