Evidence map›Paper›PMID 41068604›Full record

ArticleBMC gastroenterology2025

Elucidating the role of IgA plasma cells and PECAM1-CD38 interaction in intestinal fibrosis: a single-cell RNA sequencing analysis in Crohn's disease.

Shuyang Sun, Jiheng Wang, Kai Li, Hua Jin, Shuwen Du, Jingyan Feng, Limin Zhang, Lei Li, Yuqi He

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in BMC gastroenterology, 2025. 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. Article
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.

Shuyang Sun *Department of Gastroenterology, Beijing Chest Hospital, Capital Medical University/Beijing Tuberculosis and Thoracic Tumor Research Institute, Beijing, 101149, China.
Jiheng Wang *Department of Gastroenterology, The Seventh Medical Center of Chinese PLA General Hospital, Beijing, 100700, China.
Kai Li *Faculty of Hepato-Pancreato-Biliary Surgery, The First Medical Center of Chinese PLA General Hospital, Beijing, 100853, China.
Hua JinDepartment of Pathology, The Seventh Medical Center of Chinese PLA General Hospital, Beijing, China.
Shuwen DuDepartment of Gastroenterology, The Seventh Medical Center of Chinese PLA General Hospital, Beijing, 100700, China.
Jingyan FengSeekgene Biotechnology Co, Ltd, Beijing, China.
Limin ZhangDepartment of Gastroenterology, The Seventh Medical Center of Chinese PLA General Hospital, Beijing, 100700, China.
Lei LiDepartment of Gastroenterology, Beijing Jishuitan Hospital, Capital Medical University, Beijing, 100038, China. m13699119545@mail.ccmu.edu.cn.
Yuqi HeDepartment of Gastroenterology, Beijing Chest Hospital, Capital Medical University/Beijing Tuberculosis and Thoracic Tumor Research Institute, Beijing, 101149, China. endohe@163.com.

Funding

Beijing Municipal Science and Technology Commission No. Z171100001017145Beijing Natural Science Foundation Grant no. 7212107Capital's Funds for Health Improvement and Research Grant no. 2022-1-5082National Natural Science Foundation of China Grant no. 82273245
6 · The paper itself

Abstract

backgroundIntestinal fibrosis-associated stricture is a frequent complication of inflammatory bowel disease (IBD), often necessitating endoscopic or surgical interventions. This study aims to investigate the pathogenesis of fibrosis in Crohn's disease (CD), a type of IBD, by analyzing single-cell RNA sequencing (scRNA-Seq) data from colon biopsies of both CD and ulcerative colitis (UC) patients.

resultsThe analysis revealed significant cellular heterogeneity, altered cell-cell interactions, and key molecular pathways in both CD and UC. CD showed a marked increase in IgA plasma cells. Ligand-receptor analysis indicated that IgA plasma cells strongly interacted with inflammation-associated fibroblasts (IAFs) in CD, predominantly through the PECAM1-CD38 axis, whereas these interactions were less pronounced in UC. Our study indicated that IL-1β was upregulated in Th17 cells in CD. MAPK signaling pathway were upregulated in Th17 cells.

conclusionsThese findings may provide new insights into the mechanisms underlying early intestinal fibrosis in CD by identifying critical cell types and molecular players. Nonetheless, these observations are exploratory and will require validation in future experiments.

Indexed as

ADP-ribosyl Cyclase 1Crohn DiseaseImmunoglobulin APlasma CellsPlatelet Endothelial Cell Adhesion Molecule-1AdultColitis, UlcerativeColonFemaleFibroblastsFibrosisHumansInterleukin-1betaMaleMembrane GlycoproteinsMiddle AgedADP-ribosyl Cyclase 1CD38 protein, humanImmunoglobulin AInterleukin-1betaMembrane GlycoproteinsPECAM1 protein, humanPlatelet Endothelial Cell Adhesion Molecule-1CD38Crohn's diseaseIgA plasma cellsIL-1βInflammation-associated fibroblastsIntestinal fibrosisPECAM1Single-cell RNA sequencingUlcerative colitis

Identifiers

PMID41068604
PMCPMC12512492

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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.