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The microbiota of the mouth disperses into the lungs, and both compartments share similar phyla. Considering the importance of the microbiota in the maturation of the immunity and physiology during the first days of life, we hypothesized that primo-colonizing bacteria of the oral cavity may induce immune responses in bronchial epithelial cells. Herein, we have isolated and characterized 57 strains of the buccal cavity of two human newborns. These strains belong to , , , and genera, with being the most represented. The strains were co-incubated with a bronchial epithelial cell line (BEAS-2B), and we established their impact on a panel of cytokines/chemokines and global changes in gene expression. The strains, which appeared soon after birth, induced a high production of IL-8, suggesting they can trigger inflammation, whereas the strains were less associated with inflammation pathways. The genera , and induced differential profiles of cytokine/chemokine/growth factor and set of genes associated with maturation of morphology. Altogether, our results demonstrate that the microorganisms, primo-colonizing the oral cavity, impact immunity and morphology of the lung epithelial cells, with specific effects depending on the phylogeny of the strains.
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http://dx.doi.org/10.3390/microorganisms8081094 | DOI Listing |
Lung
September 2025
The Wellcome-Wolfson Institute for Experimental Medicine, School of Medicine, Dentistry and Biomedical Sciences, Queen's University Belfast, 97 Lisburn Road, Belfast, Belfast BT9 7BL, UK.
Introduction: Rhinovirus (RV) is the leading cause of exacerbations of lung disease. A sensory neuronal model, derived from human dental pulp stem cells and differentiated into peripheral neuronal equivalents (PNEs), was used to examine RV's effects on airway sensory nerves. We investigated whether RV can directly infect and alter PNEs or whether it exerts effects indirectly via the release of mediators from infected epithelial cells.
View Article and Find Full Text PDFBiochem Biophys Res Commun
September 2025
Selcuk University, Faculty of Medicine, Department of Medical Biochemistry, Konya, Turkey. Electronic address:
This study investigates the cytotoxic and biochemical effects of PEGylated graphene oxide sol-gel (SJ-go) nanoparticles, curcumin, and quercetin on BEAS-2B human bronchial epithelial. In this work, a new graphene oxide nanocomposite (SJ-go) was produced using the sol-gel method through a one-step reaction. These hybrid sol-gel systems include graphite, triethyl orthosilicate (TEOS), and polyethylene glycol (PEG) having a molecular weight of 8000 g/mol.
View Article and Find Full Text PDFMicrobes Infect
September 2025
Department of Pulmonary and Critical Care Medicine, The Second Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi 530007, P.R. China. Electronic address:
Background: While autophagy is pivotal in antimicrobial defense, its regulatory role in Talaromyces marneffei (TM) infected bronchial epithelium remains elusive.
Objective: To elucidate the impact of TM infection on autophagy in bronchial epithelial cells and to identify the key molecular regulators involved in this process.
Methods: Primary computational screening identified core autophagy modulators.
Front Pharmacol
August 2025
BioISI-Biosystems & Integrative Sciences Institute, Faculty of Sciences, University of Lisboa, Lisboa, Portugal.
Introduction: Cystic fibrosis (CF) is a monogenic disease caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene, which encodes a Cl/HCO ion channel located at the apical plasma membrane (PM) of epithelial cells. CFTR dysfunction disrupts epithelial barrier integrity, drives progressive airway remodelling and has been associated with epithelial-to-mesenchymal transition (EMT), a process in which cells lose epithelial properties and acquire mesenchymal characteristics. We previously demonstrated that mutant CFTR directly drives partial EMT, independently of secondary events such as bacterial infection or inflammation.
View Article and Find Full Text PDFInt Immunopharmacol
September 2025
Department of Pulmonary and Critical Care Medicine, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong 510280, China. Electronic address:
Background: Chronic obstructive pulmonary disease (COPD), mainly caused by cigarette smoke (CS), is a global health concern. Ferroptosis is recognized as a key driver of COPD progression, yet its underlying mechanisms are unclear. This study aimed to identify crucial genes involved in COPD and elucidate their functional roles in COPD via bioinformatics and experiments.
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