Evidence map›Paper›PMID 42335903›Full record

Trial reportCell reports. Medicine2026

Commensal Cutibacterium acnes-derived indolelactic acid safeguards skin barrier function through the aryl hydrocarbon receptor.

Shan Zhang, Fang Li, Xiaoqiang Xu, Tianze Yu, Yang Liu, Xiaokai Fang, Yuan Zhou, Beilei Xu, Yu Zhang, Yang Luo and 4 more

Abstract readClinical Trial
PubMed Full text at PMC Publisher
In one paragraph

Trial report in Cell reports. Medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

14 authors.

Shan ZhangDepartment of Allergy and Rheumatology, Jiangsu Provincial Key Laboratory of Dermatology, Hospital for Skin Diseases, Institute of Dermatology, Chinese Academy of Medical Sciences & Peking Union Medical College, Nanjing 210042, China; Department of Dermatology, Children's Hospital of Nanjing Medical University, Nanjing 210008, Jiangsu, China.
Fang LiDepartment of Allergy and Rheumatology, Jiangsu Provincial Key Laboratory of Dermatology, Hospital for Skin Diseases, Institute of Dermatology, Chinese Academy of Medical Sciences & Peking Union Medical College, Nanjing 210042, China.
Xiaoqiang XuDepartment of Dermatology, Shanghai Institute of Dermatology, National Clinical Research Center for Aging and Medicine, Huashan Hospital, Fudan University, Shanghai 200040, China.
Tianze YuDepartment of Dermatology, Shanghai Institute of Dermatology, National Clinical Research Center for Aging and Medicine, Huashan Hospital, Fudan University, Shanghai 200040, China.
Yang Liu01life Institute, Shenzhen 518000, China.
Xiaokai FangDepartment of Allergy and Rheumatology, Jiangsu Provincial Key Laboratory of Dermatology, Hospital for Skin Diseases, Institute of Dermatology, Chinese Academy of Medical Sciences & Peking Union Medical College, Nanjing 210042, China; Department of Dermatology, Shanghai Institute of Dermatology, National Clinical Research Center for Aging and Medicine, Huashan Hospital, Fudan University, Shanghai 200040, China.
Yuan ZhouDepartment of Allergy and Rheumatology, Jiangsu Provincial Key Laboratory of Dermatology, Hospital for Skin Diseases, Institute of Dermatology, Chinese Academy of Medical Sciences & Peking Union Medical College, Nanjing 210042, China.
Beilei XuDepartment of Allergy and Rheumatology, Jiangsu Provincial Key Laboratory of Dermatology, Hospital for Skin Diseases, Institute of Dermatology, Chinese Academy of Medical Sciences & Peking Union Medical College, Nanjing 210042, China.
Yu ZhangDepartment of Allergy and Rheumatology, Jiangsu Provincial Key Laboratory of Dermatology, Hospital for Skin Diseases, Institute of Dermatology, Chinese Academy of Medical Sciences & Peking Union Medical College, Nanjing 210042, China.
Yang LuoDepartment of Allergy and Rheumatology, Jiangsu Provincial Key Laboratory of Dermatology, Hospital for Skin Diseases, Institute of Dermatology, Chinese Academy of Medical Sciences & Peking Union Medical College, Nanjing 210042, China.
Qianjin LuDepartment of Allergy and Rheumatology, Jiangsu Provincial Key Laboratory of Dermatology, Hospital for Skin Diseases, Institute of Dermatology, Chinese Academy of Medical Sciences & Peking Union Medical College, Nanjing 210042, China.
Xiaochun LiuDepartment of Allergy and Rheumatology, Jiangsu Provincial Key Laboratory of Dermatology, Hospital for Skin Diseases, Institute of Dermatology, Chinese Academy of Medical Sciences & Peking Union Medical College, Nanjing 210042, China. Electronic address: holmes27@163.com.
Wei LiDepartment of Dermatology, Shanghai Institute of Dermatology, National Clinical Research Center for Aging and Medicine, Huashan Hospital, Fudan University, Shanghai 200040, China. Electronic address: liweiderma@fudan.edu.cn.
Xu YaoDepartment of Allergy and Rheumatology, Jiangsu Provincial Key Laboratory of Dermatology, Hospital for Skin Diseases, Institute of Dermatology, Chinese Academy of Medical Sciences & Peking Union Medical College, Nanjing 210042, China. Electronic address: dryao_xu@126.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Skin microbial dysbiosis is a key characteristic of atopic dermatitis (AD). Although Cutibacterium acnes (C. acnes) is the most abundant bacterium in the skin microbiota, its precise functions in AD remain unclear. Here, whole-genome sequencing of C. acnes isolates reveals strain-level genomic and functional heterogeneity between AD patients and healthy individuals. Metabolomic profiling identifies reduced indolelactic acid (ILA), a tryptophan metabolite, in AD skin and in cultures of AD-associated C. acnes strains. In murine models of epidermal-barrier-damaged and AD-like dermatitis, topical ILA application activates the aryl hydrocarbon receptor (AhR) pathway in keratinocytes, upregulating tight junction proteins and suppressing interleukin (IL)-33 to restore barrier integrity and mitigate dermatitis. A proof-of-concept clinical trial confirms ILA's efficacy in reducing transepidermal water loss and alleviating AD symptoms. Our study establishes C. acnes-derived ILA as a crucial regulator of skin barrier repair via AhR signaling, offering therapeutic potential for AD. Clinical trial registration: ChiCTR2400090988.

Indexed as

Dermatitis, AtopicIndolesPropionibacterium acnesReceptors, Aryl HydrocarbonSkinAnimalsFemaleHumansKeratinocytesMiceSignal TransductionSkin Microbiomeindole-3-lactic acidIndolesReceptors, Aryl Hydrocarbonatopic dermatitisCutibacterium acnesIL-33indolelactic acidtight junctions

Identifiers

PMID42335903
PMCPMC13400191

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.