ArticleJournal of inflammation research2024
PM2.5 Promotes Macrophage-Mediated Inflammatory Response Through Airway Epithelial Cell-Derived Exosomal miR-155-5p.
Article in Journal of inflammation research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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
12 citing papers in PubMed.
- The Role of MicroRNAs Implicated in the Regulation of PI3K/AKT and Focal Adhesion Signaling Pathways in Chronic Obstructive Pulmonary Disease.Biochemical genetics · 2026Article
- The triple-hit hypothesis: exploring pulmonary e-cigarette, PMEuropean respiratory review : an official journal of the European Respiratory Society · 2026Review
- The cell with many faces: lung macrophage plasticity and function in response to environmental and pathogenic insults.Physiological reviews · 2026Review
- Extracellular vesicle-mediated mechanisms and therapeutic potential in acute lung injury.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- Curcumin attenuates PM2.5-triggered pulmonary senescence via the mTOR/S6K1 signaling pathway.Biogerontology · 2026Article
- Exosomal miR-2110 from PM2.5-Exposed Lung Epithelial Cells Targets SRSF1 to Promote M1 Macrophage Polarization and Inflammatory Responses in COPD.International journal of chronic obstructive pulmonary disease · 2026Article
- Smoking accelerates immunosenescence in multiple sclerosis.Frontiers in immunology · 2026Review
- Exosomal miRNAs: A New Frontier in Cardiovascular Disease Diagnosis and Treatment.Journal of cardiovascular translational research · 2025Review
- Epithelial Cell Dysfunction in Pulmonary Fibrosis: Mechanisms, Interactions, and Emerging Therapeutic Targets.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Association between low-concentration PMFrontiers in public health · 2025Article
- PM2.5 Induces Cell-Specific Transcriptomic Alterations in the Lungs of Juvenile Mice.Journal of inflammation research · 2025Article
- Role and mechanism of IGFBP5 in the real-ambient particulate matter exposure-induced chronic lung injury.Frontiers in pharmacology · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Airway epithelial cells (AECs) and alveolar macrophages are involved in airway inflammation. The direct effects of atmospheric fine-particulate-matter (PM2.5) on airway cells, such as AECs and alveolar macrophages, have been widely investigated, but the effect of cell-cell interaction on inflammatory response remains unclear. Exosomes play a crucial role in intercellular communication. However, the cellular interaction of exosomes in PM2.5-induced airway inflammation is unclear. Methods: The PM2.5-induced human bronchial epithelial (BEAS-2B) cells and phorbol 12-myristate 13-acetate-induced macrophages (Mφ) were co-cultured and then the expression of IL-6, IL-1β, TNF-α and miRNA-155-5p were detected. Exosomes from PM2.5-exposed BEAS-2B cells were then co-cultured with Mφ to detect the expression of miR-155-5p and inflammatory cytokines, as well as cytokine signaling inhibitor-1 (SOCS1)/NFκB, and to detect the effect of the exosome inhibitor GW4869. Results: After the co-culture of PM2.5-induced BEAS-2B cells and Mφ, the expression of Mφ-derived IL-6, IL-1β, and TNF-α, as well as miRNA-155-5p were upregulated. The expression of miRNA-155-5p was upregulated in BEAS-2B and BEAS-2B cell-derived exosomes after exposure to PM2.5. Furthermore, co-culturing exosomes derived from PM2.5-exposed BEAS-2B cells with Mφ, upregulated miR-155-5p and inflammatory cytokines, decreased cytokine signaling inhibitor-1 (SOCS1) expression, and activated NF-κB. In addition, adding exosome inhibitor GW4869 to PM2.5-interfered BEAS-2B cells co-culture with Mφ downregulated miRNA-155-5p expression, inhibited NF-κB, and reduced the levels of inflammatory factors. Conclusion: PM2.5 promotes Mφ inflammation by upregulating miRNA-155-5P in exosomes obtained from BEAS-2B cells through miR-155-5P/SOCS1/NF-κB pathway. Exosomal miRNAs mediate cellular communication between BEAS-2B cells and Mφ, which may be a new mechanism of PM2.5-stimulated pulmonary inflammatory response.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.