Evidence map›Paper›PMID 41823703›Full record

ArticleThe ISME journal2026

Cellular membrane protein MipA from E.coli Nissle 1917 protects against Salmonella infection.

Yunqing Xiang, Huipai Peng, Yanxia Li, Hui Wen, Nan Li, Xiaozhi Liu, Guodong Yuan, Yong Shi, Shuqiang Huang

Abstract read
In one paragraph

Article in The ISME journal, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. 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

9 authors.

Yunqing XiangState Key Laboratory of Quantitative Synthetic Biology, Shenzhen Institute of Synthetic Biology, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen, Guangdong 518055, China.
Huipai PengState Key Laboratory of Quantitative Synthetic Biology, Shenzhen Institute of Synthetic Biology, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen, Guangdong 518055, China.
Yanxia LiTianjin Key Laboratory of Epigenetics for Organ Development of Premature Infants, Tianjin Fifth Central Hospital, Tianjin 300450, China.
Hui WenState Key Laboratory of Quantitative Synthetic Biology, Shenzhen Institute of Synthetic Biology, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen, Guangdong 518055, China.
Nan LiState Key Laboratory of Quantitative Synthetic Biology, Shenzhen Institute of Synthetic Biology, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen, Guangdong 518055, China.
Xiaozhi LiuTianjin Key Laboratory of Epigenetics for Organ Development of Premature Infants, Tianjin Fifth Central Hospital, Tianjin 300450, China.
Guodong YuanState Key Laboratory of Superlattices and Microstructures, Institute of Semiconductors, Chinese Academy of Sciences, Beijing 100083, China.
Yong ShiDepartment of Mechanical, Materials and Manufacturing Engineering, University of Nottingham Ningbo China, Ningbo 315100, China.
Shuqiang HuangState Key Laboratory of Quantitative Synthetic Biology, Shenzhen Institute of Synthetic Biology, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen, Guangdong 518055, China.

Funding

Strategic Priority Research Program of the Chinese Academy of Sciences XDA0510200
6 · The paper itself

Abstract

Intestinal microbiota resists pathogenic bacterial infections through colonization resistance, largely attributed to direct microbial competition. However, whether commensals can provide colonization resistance by remodeling the host epithelial niche remains underexplored. Here, by combining in vivo mouse models and a gut-on-chip model, this study demonstrates that the resistance of commensal Escherichia coli Nissle 1917 (EcN) against Salmonella Typhimurium (STm) infection is strictly dependent on EcN precolonization. Mechanistically, the EcN outer membrane protein MipA was identified as a key factor that induces the upregulation of integrin-linked kinase (ILK), thereby reinforcing tight junction integrity and restricting Salmonella infection. Engineering a nonprotective strain to express MipA was sufficient to confer resistance against Salmonella infection. This work reveals an epithelial defense mechanism triggered by a specific probiotic protein, with implications for developing preventive strategies against enteric infections.

Indexed as

Bacterial Outer Membrane ProteinsEscherichia coliEscherichia coli ProteinsSalmonella InfectionsSalmonella typhimuriumAnimalsDisease Models, AnimalHumansMiceProbioticsProtein Serine-Threonine KinasesScaffold Protein ILKTight JunctionsBacterial Outer Membrane ProteinsEscherichia coli ProteinsProtein Serine-Threonine KinasesScaffold Protein ILKcolonization resistancegut-on-chiphost–microbe interactionprobiotics

Identifiers

PMID41823703
PMCPMC13077295

What OpenQuestion 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 OpenQuestion graph.