ArticleJournal of biomedical science2025
Goblet cell breakdown: transcriptomics reveals Acinetobacter baumannii early and robust inflammatory response in differentiated human bronchial epithelial cells.
Article in Journal of biomedical science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Obstructive fibrinous tracheal pseudomembrane complicated with bronchial mucus plug: A rare post-intubation complication case report.Journal of anesthesia and translational medicine · 2026Article
- Respiratory Models Reveal DNA Damage Response Modulation by Merkel Cell Polyomavirus.International journal of molecular sciences · 2026Article
- Exploring the Anti-Cervical Cancer Effect and Hepatotoxicity Risk of Gossypol Based on Untargeted Metabolomics and Network Toxicology.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Inside Enemy Lines: Adhesion, Invasion, and Intracellular Persistence ofPathogens (Basel, Switzerland) · 2026Review
- Study on the anti-inflammatory effects and mechanisms of gentisic acid based on the LPS-induced RAW264.7 cell inflammation model and the oxazolone-induced zebrafish inflammation model.Frontiers in pharmacology · 2026Article
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Authors and funding
11 authors.
Funding
Abstract
backgroundThe airway epithelium represents the first line of defense of the lungs, functioning both as a physical barrier as well as an active immune modulator. However, in the last years, pneumonia caused by the opportunistic pathogen Acinetobacter baumannii have become difficult to treat due to the increase of the number of extensively drug resistant strains. In this study, we report for the first time the use of an ex vivo air-liquid interface (ALI) model of differentiated human bronchial epithelial cells to unravel the early response to A. baumannii infection.
methodsEpithelial integrity, tissue architecture, and goblet cell function were assessed through FITC-dextran permeability assays, hematoxylin and eosin staining, and indirect immunofluorescence. Transcriptomic profiling was performed to characterize host gene expression changes.
resultsInitial tissue damage began as early as at 4 h post-infection (hpi); at 24 hpi, goblet cell hypertrophy, reduced mucin secretion, and compromised epithelial integrity were highly evident. Transcriptomic data at 4 hpi revealed 668 differentially expressed genes (441 upregulated, 227 downregulated), mainly involved in a strong pro-inflammatory response and characterized by IL-8/CCL20-driven neutrophil recruitment and type 2 cytokine activation (IL-4, IL-13). Noteworthy, genes related to cytoskeletal organization, adhesion, and extracellular matrix remodeling were significantly altered, suggesting a bacterial mechanism to enhanced tissue dissemination. The PI3K-Akt survival pathway was inhibited, with downregulation of PIK3R1 and PIK3R2 genes, implying the induction of apoptosis/cell death and epithelial damage. Our findings are in agreement with previous in vivo studies, further strengthening the value of our ALI model in mimicking the early infection response of bronchial cells to A. baumannii infection.
conclusionOur data highlight the early molecular mechanisms underlying A. baumannii pathogenesis and open new avenues for future investigations for therapeutic interventions.
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