ArticleJournal of extracellular vesicles2026
Extracellular Vesicles Coordinate Bacterial Cloaking in Lung Epithelial Cells to Alleviate Acute Inflammatory Injury.
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.
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.
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.
Who cites it
1 citing paper in PubMed.
- Extracellular Vesicles Coordinate Bacterial Cloaking in Lung Epithelial Cells to Alleviate Acute Inflammatory Injury.Journal of extracellular vesicles · 2026Article
Corrections and comments
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Authors and funding
16 authors.
Funding
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.
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Registered trials
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.