ArticleNature communications2025
Volatile and non-volatile pathogen cues shape host extracellular vesicles production in pre-infection response.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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
2 citing papers in PubMed.
- Mechanisms and functions of large extracellular vesicle biogenesis.Nature cell biology · 2026Review
- Modulation of host proteostasis by Prevotella corporis via induction of the heat shock response.Cell stress & chaperones · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
Abstract
In natural environments, animals encounter pathogen-derived chemicals long before infection occurs. How such anticipatory cues influence extracellular vesicle (EV) dynamics, which are central to immune regulation, intercellular communication, and stress responses, remains unknown. Using Caenorhabditis elegans, we show that pathogen-derived volatile and non-volatile compounds trigger distinct EV pathways through separate sensory and molecular mechanisms. Non-volatile secretome components, including the tripeptide Ile-Pro-Pro, activate immune-dependent EV production, whereas volatile metabolites elicit immunity-independent EV formation. Both responses require sensory input from ASK, ADL, and AWC neurons and converge on a neural circuit involving RMG, AIB, and AIA interneurons. GPCRs SRI-19, SRI-36/39, and SRR-6 mediate non-volatile responses, with SRR-6 acting in the intestine to regulate muscle EVs release. Notably, pre-exposure to pathogen volatiles enhances offspring survival during subsequent infection in an SRI-19-dependent manner, suggesting a predictive, intergenerational benefit of pathogen detection. In summary, our findings uncover that pathogen-derived chemical cues shape host EV production via specialized sensory circuits, revealing how animals anticipate infection and prime protective physiological responses.
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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.