Evidence map›Paper›PMID 41656978›Full record

ArticleJournal of extracellular vesicles2026

Extracellular Vesicles Coordinate Bacterial Cloaking in Lung Epithelial Cells to Alleviate Acute Inflammatory Injury.

Feng Ding, Shengkai Gong, Haotian Luo, Dandan Wu, Xiaoshan Yang, Zihan Li, Dingmei Zhang, Peijie He, Jiani Liu, Lili Bao and 6 more

Abstract read
In one paragraph

Article in Journal of extracellular vesicles, 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. 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

16 authors.

Feng DingState Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, National Clinical Research Center for Oral Diseases, Shaanxi Key Laboratory of Stomatology, Department of Oral Biology & Clinic of Oral Rare Diseases and Genetic Disease, School of Stomatology, The Fourth Military Medical University, Xi'an, Shaanxi, China.ORCID https://orcid.org/0000-0001-5973-180X
Shengkai GongState Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, National Clinical Research Center for Oral Diseases, Shaanxi Key Laboratory of Stomatology, Department of Oral Biology & Clinic of Oral Rare Diseases and Genetic Disease, School of Stomatology, The Fourth Military Medical University, Xi'an, Shaanxi, China.
Haotian LuoState Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, National Clinical Research Center for Oral Diseases, Shaanxi Key Laboratory of Stomatology, Department of Oral Biology & Clinic of Oral Rare Diseases and Genetic Disease, School of Stomatology, The Fourth Military Medical University, Xi'an, Shaanxi, China.
Dandan WuState Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, National Clinical Research Center for Oral Diseases, Shaanxi Key Laboratory of Stomatology, Department of Radiology, School of Stomatology, The Fourth Military Medical University, Xi'an, Shaanxi, China.
Xiaoshan YangState Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, National Clinical Research Center for Oral Diseases, Shaanxi Key Laboratory of Stomatology, Department of Oral Biology & Clinic of Oral Rare Diseases and Genetic Disease, School of Stomatology, The Fourth Military Medical University, Xi'an, Shaanxi, China.
Zihan LiState Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, National Clinical Research Center for Oral Diseases, Shaanxi Key Laboratory of Stomatology, Department of Oral Biology & Clinic of Oral Rare Diseases and Genetic Disease, School of Stomatology, The Fourth Military Medical University, Xi'an, Shaanxi, China.
Dingmei ZhangState Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, National Clinical Research Center for Oral Diseases, Shaanxi Key Laboratory of Stomatology, Department of Oral Biology & Clinic of Oral Rare Diseases and Genetic Disease, School of Stomatology, The Fourth Military Medical University, Xi'an, Shaanxi, China.
Peijie HeState Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, National Clinical Research Center for Oral Diseases, Shaanxi Key Laboratory of Stomatology, Department of Periodontology, School of Stomatology, The Fourth Military Medical University, Xi'an, Shaanxi, China.
Jiani LiuState Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, National Clinical Research Center for Oral Diseases, Shaanxi Key Laboratory of Stomatology, Digital Center, School of Stomatology, The Fourth Military Medical University, Xi'an, Shaanxi, China.
Lili BaoState Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, National Clinical Research Center for Oral Diseases, Shaanxi Key Laboratory of Stomatology, Department of Oral Biology & Clinic of Oral Rare Diseases and Genetic Disease, School of Stomatology, The Fourth Military Medical University, Xi'an, Shaanxi, China.
Yang ZhouState Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, National Clinical Research Center for Oral Diseases, Shaanxi Key Laboratory of Stomatology, Department of Oral Biology & Clinic of Oral Rare Diseases and Genetic Disease, School of Stomatology, The Fourth Military Medical University, Xi'an, Shaanxi, China.
Zhengyan WangState Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, National Clinical Research Center for Oral Diseases, Shaanxi Key Laboratory of Stomatology, Department of Oral Biology & Clinic of Oral Rare Diseases and Genetic Disease, School of Stomatology, The Fourth Military Medical University, Xi'an, Shaanxi, China.
Siying LiuState Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, National Clinical Research Center for Oral Diseases, Shaanxi Key Laboratory of Stomatology, Department of Orthodontics, School of Stomatology, The Fourth Military Medical University, Xi'an, Shaanxi, China.
Pei WangState Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, National Clinical Research Center for Oral Diseases, Shaanxi Key Laboratory of Stomatology, Department of Radiology, School of Stomatology, The Fourth Military Medical University, Xi'an, Shaanxi, China.
Geng DouState Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, National Clinical Research Center for Oral Diseases, Shaanxi Key Laboratory of Stomatology, Department of Oral Biology & Clinic of Oral Rare Diseases and Genetic Disease, School of Stomatology, The Fourth Military Medical University, Xi'an, Shaanxi, China.
Shiyu LiuState Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, National Clinical Research Center for Oral Diseases, Shaanxi Key Laboratory of Stomatology, Department of Oral Biology & Clinic of Oral Rare Diseases and Genetic Disease, School of Stomatology, The Fourth Military Medical University, Xi'an, Shaanxi, China.ORCID https://orcid.org/0000-0001-7972-4527

Funding

China Postdoctoral Science Foundation 2023M734280National Natural Science Foundation of China 82170925National Natural Science Foundation of China 82301027National Natural Science Foundation of China 82301099National Natural Science Foundation of China 82470947National Natural Science Foundation of China 82471012National Natural Science Foundation of China 82502730Shaanxi Provincial Key Research and Development Program 2024SF-GJHX-29
6 · The paper itself

Abstract

The capacity of host professional phagocytes to attenuate excessive inflammatory responses through pathogen cloaking during infection has been well-established. However, the involvement of non-professional phagocytes in this process remains unknown. Here, we identify a previously unrecognized mechanism by which lung epithelial cells (LECs) attenuate inflammatory responses during Staphylococcus aureus infection. S. aureus-challenged LECs rapidly shed extracellular vesicles (EVs) carrying surface receptors capable of binding invading bacteria and forming EV-bacteria complexes. The EV-bacteria complexes were internalized by LECs via RhoA-ROCK1-actin-driven endocytosis pathway, reducing free bacterial burden within the alveolar lumen. This EV-mediated pathogen cloaking conferred acute-phase protection, as demonstrated by mitigating early-stage pulmonary inflammation, and improving survival rates in infected mice. Paradoxically, this strategy permitted chronic bacterial persistence and sustaining low-grade inflammation. Our findings delineate a trade-off mechanism that non-professional phagocytes modulate acute bacterial infection and inflammatory responses via pathogen cloaking. This mechanistic perspective reframes non-professional phagocytes as active architects of infection outcomes based on EV-mediated host-pathogen interactions. Our work provides insights into the mechanism of bacterial cloaking during infection and suggests stage-specific therapeutic strategies.

Indexed as

Epithelial CellsExtracellular VesiclesInflammationLungStaphylococcal InfectionsStaphylococcus aureusAnimalsHost-Pathogen InteractionsHumansMicePhagocytesacute bacterial infectionEV‐bacteria complexesextracellular vesiclespathogen cloakingStaphylococcus aureus

Identifiers

PMID41656978
PMCPMC12884003

What OpenQuestion holds

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LicenceCC BY
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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.