Evidence map›Paper›PMID 42174415›Full record

ArticleBMC microbiology2026

Lineage-specific type 1 fimbriae in hypervirulent ST23 Klebsiella pneumoniae target α3β1 integrin to promote intestinal epithelial invasion.

Qian Zeng, Ying Zhang, Shujing Li, Xinyue Fan, Su Wang, Jiayuan Liu, Cui Tai, Meng Li, Yuanyuan Wei, Yunkun Huang and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in BMC microbiology, 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

13 authors.

Qian Zeng *Department of Laboratory Medicine, Huashan Hospital, Fudan University, Shanghai, China.
Ying Zhang *Department of Laboratory Medicine, Huashan Hospital, Fudan University, Shanghai, China.
Shujing Li *Department of Laboratory Medicine, Huashan Hospital, Fudan University, Shanghai, China.
Xinyue Fan *Department of Laboratory Medicine, Huashan Hospital, Fudan University, Shanghai, China.
Su WangDepartment of Laboratory Medicine, Huadong Hospital, Fudan University, Shanghai, China.
Jiayuan LiuSchool of Pharmaceutical Science and Technology, Hangzhou Institute for Advanced Study, University of Chinese Academy of Sciences, Hangzhou, China.
Cui TaiState Key Laboratory of Microbial Metabolism, School of Life Sciences & Biotechnology, Shanghai Jiao Tong University, Shanghai, China.
Meng LiDepartment of Clinical Laboratory, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, China.
Yuanyuan WeiDepartment of Clinical Laboratory, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, China.
Yunkun HuangDepartment of Clinical Laboratory, The Affiliated Yan'an Hospital of Kunming Medical University, Kunming, Yunnan, China.
Yi LiDepartment of Laboratory Medicine, Henan Provincial People's Hospital, Zhengzhou University, Zhengzhou, Henan, China.
Lefu LanSchool of Pharmaceutical Science and Technology, Hangzhou Institute for Advanced Study, University of Chinese Academy of Sciences, Hangzhou, China. llan@ucas.ac.cn.
Xiaofei JiangDepartment of Laboratory Medicine, Huashan Hospital, Fudan University, Shanghai, China. jiangxi2154@sina.com.

Funding

National Natural Science Foundation of China 82372310 and 82172315
6 · The paper itself

Abstract

Hypervirulent Klebsiella pneumoniae (hvKp), particularly sequence type 23 (ST23), is a predominant global cause of pyogenic liver abscesses. While ST23 hvKp is strongly associated with this invasive pathology, the molecular basis for its enhanced gut translocation potential, a critical prerequisite for hematogenous dissemination to the liver, remains unclear. Phylogenetic analysis of type 1 fimbrial gene clusters revealed that ST23 isolates uniquely encode a distinct combination of fimbrial subunits. Using engineered strains, we demonstrated that ST23-derived type 1 fimbriae, but not those from the ST11 lineage of classical K. pneumoniae, specifically bind to host enterocyte α3β1 integrins. This specific interaction conferred superior invasion capacity across intestinal epithelial barriers to ST23 hvKp compared to strains expressing ST11 fimbriae (P < 0.05). Thus, ST23 hvKp exploits lineage-specific type 1 fimbriae to target α3β1 integrin, driving efficient gut epithelial invasion-a pivotal initial step in systemic dissemination leading to liver abscess formation. This work identifies a dedicated molecular invasion system intrinsic to ST23 hvKp, mechanistically explaining its enhanced invasive capacity and strong clinical association with pyogenic liver abscesses.

Indexed as

Fimbriae, BacterialIntegrin alpha3beta1Intestinal MucosaKlebsiella InfectionsKlebsiella pneumoniaeAnimalsBacterial AdhesionEnterocytesEpithelial CellsHumansLiver Abscess, PyogenicMultigene FamilyPhylogenyVirulenceIntegrin alpha3beta1FimH-integrin interactionIntegrin-mediated invasionLiver abscess pathogenesisST23 hypervirulent Klebsiella pneumoniaeType 1 fimbriae

Identifiers

PMID42174415
PMCPMC13349070

What OpenQuestion holds

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Registered trials

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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.