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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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Asthma-II: Pathophysiology and Classification01:26

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Refined Murine Model of Idiopathic Pulmonary Fibrosis
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Rhinovirus-induced basic fibroblast growth factor release mediates airway remodeling features.

Chrysanthi L Skevaki1, Stelios Psarras, Eleni Volonaki

  • 1UPC Research Laboratories, Allergy Department, 2nd Pediatric Clinic, University of Athens, 41 Fidipidou str, Athens, 115 27, Greece. cskevaki@allergy.gr.

Clinical and Translational Allergy
|August 23, 2012
PubMed
Summary

Human rhinovirus infections trigger airway remodeling in asthma by increasing basic fibroblast growth factor (bFGF). This promotes lung fibroblast proliferation, potentially worsening asthma persistence, especially in atopic individuals.

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Published on: May 26, 2023

Area of Science:

  • Respiratory Medicine
  • Immunology
  • Cell Biology

Background:

  • Human rhinoviruses are primary triggers for asthma exacerbations, causing airway inflammation and angiogenesis.
  • This study investigated the potential role of rhinoviruses in the fibrotic aspects of airway remodeling in asthma.

Purpose of the Study:

  • To determine if rhinoviruses contribute to airway remodeling through fibrotic processes.
  • To assess the role of basic fibroblast growth factor (bFGF) in rhinovirus-induced airway changes.

Main Methods:

  • Measured bFGF mRNA and protein levels after rhinovirus infection of bronchial epithelial cells.
  • Assessed epithelial product profibrotic effects using DNA synthesis and matrix metalloproteinase assays.
  • Evaluated bFGF release from peripheral blood mononuclear cells exposed to rhinovirus and measured bFGF in respiratory secretions during asthma exacerbations.

Main Results:

  • Rhinovirus infection increased bFGF mRNA and release from epithelial cells, correlated with cytotoxicity.
  • Epithelial products induced lung fibroblast proliferation, inhibited by anti-bFGF antibody, and increased matrix metalloproteinase activity.
  • bFGF release was higher in atopic asthma models and during rhinovirus-associated asthma exacerbations.

Conclusions:

  • Rhinovirus infection stimulates airway epithelial bFGF release, promoting fibroblast proliferation and airway remodeling in asthma.
  • Recurrent rhinovirus infections may perpetuate asthma, particularly in atopic individuals.
  • Preventing rhinovirus infections could potentially alter the long-term course of asthma.