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Chronic Obstructive Pulmonary Disease III: Chronic Bronchitis Features01:24

Chronic Obstructive Pulmonary Disease III: Chronic Bronchitis Features

Chronic bronchitis is a key phenotype of chronic obstructive pulmonary disease (COPD), characterized by airway-centered inflammation and mucus overproduction. It develops from long-term exposure to harmful particles or gases, most commonly cigarette smoke, which triggers a persistent inflammatory response.Cellular and Structural ChangesInflammation initially affects the large bronchi and later the smaller airways, with infiltration by immune cells, including neutrophils, macrophages, and...

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Modeling Chronic BaP Exposure in Bronchial Epithelial Cells Reveals Multi-Scale Drivers of Early Preneoplastic

Cristian Andrade-Madrigal1, Cecilia Rojas-Fuentes2,3,4, Javier Díaz-Mijares2,3

  • 1Laboratory of Oncovirology, Departamento de Ciencias Biomédicas, Facultad de Medicina, Universidad de Tarapacá, Arica 1000000, Chile.

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|March 27, 2026
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Summary

Chronic exposure to benzo[a]pyrene (BaP) causes lung preneoplastic changes in bronchial cells. This study reveals how BaP reprograms cells, leading to dysplasia and disrupted polarity, crucial for understanding lung cancer initiation.

Keywords:
ALIATMBEAS-2B cellsBPDEDDRbenzo[a]pyrenechronic exposurelung carcinogenesisphospho-arraystranscriptomicsγ-H2AX

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Area of Science:

  • Environmental Toxicology
  • Molecular Carcinogenesis
  • Cell Biology

Background:

  • Chronic exposure to benzo[a]pyrene (BaP), a known carcinogen, is a significant factor in lung cancer development.
  • The precise mechanisms by which sustained, sub-lethal BaP exposure transforms bronchial epithelium into preneoplastic states are not fully understood.

Purpose of the Study:

  • To investigate the long-term effects of environmentally relevant benzo[a]pyrene concentrations on human bronchial epithelial cells.
  • To elucidate the molecular and cellular reprogramming events induced by chronic BaP exposure that contribute to lung carcinogenesis initiation.

Main Methods:

  • Exposure of BEAS-2B cells to continuous benzo[a]pyrene (0.1 and 1.0 µM) for 12 weeks.
  • Integrated multi-omics analysis including functional toxicology, RT-qPCR, RNA-seq, phospho-kinase/NF-κB arrays.
  • Assessment using organotypic air-liquid interface (ALI) cultures for 3D modeling.

Main Results:

  • Sustained CYP1A1/CYP1B1 induction and accumulating genotoxic stress (γ-H2AX, ATM phosphorylation) without loss of metabolic competence.
  • Dose-dependent transcriptional shifts with altered extracellular matrix, cell adhesion, inflammatory, and signaling pathways.
  • Activation of p53/NF-κB, MAPK/ERK, and PI3K/Akt pathways; ALI cultures showed histological dysplasia and polarity disruption.

Conclusions:

  • Chronic BaP exposure mechanistically links to an initiation-like preneoplastic state in bronchial epithelium.
  • BaP-induced genotoxic stress and signaling pathway activation contribute to cellular reprogramming.
  • A validated 2D/3D multi-omics platform is established for studying polycyclic aromatic hydrocarbon-driven lung carcinogenesis.