Evidence map›Paper›PMID 41824764›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026

Endogenous Ceramide 24:1 Constrains Th17-Driven Neutrophilic Inflammation by Antagonizing EP2 Signaling.

Huan Liu, Abudureyimujiang Aili, Zheng Kuang, Liting Cao, Zemin Li, Ying Shang, Yingying Ge, Tingting Hu, Yongchang Sun, Wuli Zhao and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 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

12 authors.

Huan LiuDepartment of Respiratory and Critical Care Medicine, Peking University Third Hospital, Beijing, China.
Abudureyimujiang AiliDepartment of Medical Oncology and Radiation Sickness, Peking University Third Hospital, Beijing, China.
Zheng KuangDepartment of Immunology, Peking University Health Science Center, Peking University Center for Human Disease Genomics, Beijing, China.
Liting CaoDepartment of Respiratory and Critical Care Medicine, Peking University Third Hospital, Beijing, China.
Zemin LiDepartment of Respiratory and Critical Care Medicine, Peking University Third Hospital, Beijing, China.
Ying ShangDepartment of Respiratory and Critical Care Medicine, Peking University Third Hospital, Beijing, China.
Yingying GeDepartment of Respiratory and Critical Care Medicine, Peking University Third Hospital, Beijing, China.
Tingting HuDepartment of Respiratory and Critical Care Medicine, Peking University Third Hospital, Beijing, China.
Yongchang SunDepartment of Respiratory and Critical Care Medicine, Peking University Third Hospital, Beijing, China.
Wuli ZhaoState Key Laboratory of Respiratory Health and Multimorbidity, Key Laboratory of Antibiotic Bioengineering, Laboratory of Oncology, Institute of Medicinal Biotechnology, Ministry of Health, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.
Rong JinDepartment of Immunology, School of Basic Medical Sciences, Medicine Innovation Center for Fundamental Research on Major Immunology-Related Diseases, NHC Key Laboratory of Medical Immunology (Peking University), Peking University, Beijing, China.
Chun ChangDepartment of Respiratory and Critical Care Medicine, Peking University Third Hospital, Beijing, China.ORCID https://orcid.org/0000-0003-1362-5950

Funding

Capital's Funds for Health Improvement and Research 2024-3-40917Chinese Academy of Medical Sciences Innovation Fund for Medical Sciences 2023-I2M-2-001Chinese Academy of Medical Sciences Innovation Fund for Medical Sciences 2025-I2M-KJ-019Key Clinical Projects of Peking University Third Hospital BYSYZD2023009National Natural Science Foundation of China 32071178National Natural Science Foundation of China 81902909National Natural Science Foundation of China 82170028National Natural Science Foundation of China 82370032Natural Science Foundation of Beijing Municipality 7232205Peking University Third Hospital's Cohort Construction Project BYSYDL2021020State Key Laboratory Special Fund 2060204
6 · The paper itself

Abstract

Dysregulated chronic inflammation underlies a spectrum of severe asthma phenotypes, among which neutrophilic asthma (NA) represents a treatment-recalcitrant endotype characterized by Th17-driven airway inflammation and steroid resistance. Although lipid mediators are known to play dual roles in promoting and resolving inflammation, the lipid species governing the Th17-neutrophil axis in NA remain unknown. Here, through integrated lipidomic profiling of clinical samples (exhaled breath condensate, plasma, sputum) from an NA cohort and a murine model of Th17-driven airway inflammation, a deficiency in very-long-chain ceramides, notably Cer24:1, was identified. This reduction correlated with disease severity and neutrophilic inflammation. In vivo, Cer24:1 supplementation alleviated airway hyperresponsiveness and neutrophilic infiltration, while Smpd1 knockout mice-with impaired ceramide generation-displayed exacerbated Th17 pathology. Using structure-guided molecular docking, surface plasmon resonance, and functional assays, Cer24:1 was shown to directly target the prostaglandin E2 receptor EP2 on CD4

Indexed as

AsthmaCeramidesInflammationNeutrophilsReceptors, Prostaglandin E, EP2 SubtypeTh17 CellsAnimalsDisease Models, AnimalHumansMiceMice, KnockoutSignal TransductionCeramidesReceptors, Prostaglandin E, EP2 Subtypeceramideneutrophilic asthmasphingolipidsTh17 cells

Identifiers

PMID41824764
PMCPMC13205653

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.