ArticleJournal of extracellular vesicles2026
Clostridioides difficile-Derived Extracellular Vesicles Induce Proinflammatory Responses in Macrophages.
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 3 papers.
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
3 citing papers in PubMed.
- Sub-inhibitory concentrations of metronidazole alter the proteomic profile and biological effects of extracellular vesicles from Clostridioides difficile.BMC microbiology · 2026Article
- Cytoplasmic membrane vesicles fromFrontiers in microbiology · 2026Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors.
Funding
Abstract
Clostridioides difficile (CD) is a leading cause of antibiotic-associated diarrhoea in both hospitalized and non-hospitalized patients. This study explores the role of extracellular vesicles (EVs) derived from Clostridioides difficile strain 630 (CD630-EVs), which released spherical EVs during in vitro culture, in modulating pro-inflammatory cytokine production in macrophages. Proteomic analysis identified a total of 1064 proteins within CD630-EVs, including four immune-related proteins: FliC, TrxA, TrxA2 and HtpG. Notably, FliC exhibited the highest expression intensity within immune-related pathways. CD630-EVs significantly stimulated the production of inflammatory factors, such as interleukin (IL)-6, monocyte chemoattractant protein-1 (MCP-1), IL-1α and TNF-α, in mouse macrophages. However, the addition of TH1020, a flagellin receptor inhibitor, markedly suppressed cytokine production. Protein docking analysis further demonstrated that TH1020 disrupts the interaction between Toll-Like Receptor 5 (TLR5) and FliC, thereby attenuating FliC-mediated inflammatory responses in macrophages. FliC likely plays a pivotal role in mediating the inflammatory response induced by CD630-EVs in macrophages. This effect is potentially driven by the activation of innate immunity through FliC's interaction with TLR5 in the host, which may subsequently influence adaptive immune responses. In conclusion, this study elucidates the immune-modulatory effects of CD630-EVs on host macrophages during Clostridioides difficile infection (CDI). CD630-EVs contain a diverse array of proteins, with FliC emerging as a key mediator of pro-inflammatory responses in macrophages. These findings suggest that FliC may play a critical role in intestinal mucosal injury during CDI, highlighting its potential as a therapeutic target for mitigating inflammation in CDI.
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What Socratic holds
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 Socratic graph.