Airway basal cells: The "smoking gun" of chronic obstructive pulmonary disease

Research output: Contribution to journalReview article

34 Citations (Scopus)

Abstract

The earliest abnormality in the lung associated with smoking is hyperplasia of airway basal cells, the stem/progenitor cells of the ciliated and secretory cells that are central to pulmonary host defense. Using cell biology and 'omics technologies to assess basal cells isolated from bronchoscopic brushings of nonsmokers, smokers, and smokers with chronic obstructive pulmonary disease (COPD), compelling evidence has been provided in support of the concept that airway basal cells are central to the pathogenesis of smoking-associated lung diseases. When confronted by the chronic stress of smoking, airway basal cells become disorderly, regress to a more primitive state, behave as dictated by their inheritance, are susceptible to acquired changes in their genome, lose the capacity to regenerate the epithelium, are responsible for the major changes in the airway that characterize COPD, and, with persistent stress, can undergo malignant transformation. Together, these observations led to the conclusion that accelerated loss of lung function in susceptible individuals begins with disordered airway basal cell biology (i.e., that airway basal cells are the "smoking gun" of COPD, a potential target for the development of therapies to prevent smoking-related lung disorders).

Original languageEnglish
Pages (from-to)1355-1362
Number of pages8
JournalAmerican Journal of Respiratory and Critical Care Medicine
Volume190
Issue number12
DOIs
Publication statusPublished - 1 Jan 2014
Externally publishedYes

Fingerprint

Chronic Obstructive Pulmonary Disease
Smoking
Lung
Cell Biology
Stem Cells
Lung Diseases
Hyperplasia
Epithelium
Genome
Technology
Therapeutics

Keywords

  • Airway epithelium
  • Basal cells
  • COPD
  • Lung cancer
  • Smoking

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine
  • Critical Care and Intensive Care Medicine

Cite this

Airway basal cells : The "smoking gun" of chronic obstructive pulmonary disease. / Crystal, Ronald.

In: American Journal of Respiratory and Critical Care Medicine, Vol. 190, No. 12, 01.01.2014, p. 1355-1362.

Research output: Contribution to journalReview article

@article{58db34e0661d406b8f2fdf1b4959565d,
title = "Airway basal cells: The {"}smoking gun{"} of chronic obstructive pulmonary disease",
abstract = "The earliest abnormality in the lung associated with smoking is hyperplasia of airway basal cells, the stem/progenitor cells of the ciliated and secretory cells that are central to pulmonary host defense. Using cell biology and 'omics technologies to assess basal cells isolated from bronchoscopic brushings of nonsmokers, smokers, and smokers with chronic obstructive pulmonary disease (COPD), compelling evidence has been provided in support of the concept that airway basal cells are central to the pathogenesis of smoking-associated lung diseases. When confronted by the chronic stress of smoking, airway basal cells become disorderly, regress to a more primitive state, behave as dictated by their inheritance, are susceptible to acquired changes in their genome, lose the capacity to regenerate the epithelium, are responsible for the major changes in the airway that characterize COPD, and, with persistent stress, can undergo malignant transformation. Together, these observations led to the conclusion that accelerated loss of lung function in susceptible individuals begins with disordered airway basal cell biology (i.e., that airway basal cells are the {"}smoking gun{"} of COPD, a potential target for the development of therapies to prevent smoking-related lung disorders).",
keywords = "Airway epithelium, Basal cells, COPD, Lung cancer, Smoking",
author = "Ronald Crystal",
year = "2014",
month = "1",
day = "1",
doi = "10.1164/rccm.201408-1492PP",
language = "English",
volume = "190",
pages = "1355--1362",
journal = "American Journal of Respiratory and Critical Care Medicine",
issn = "1073-449X",
publisher = "American Thoracic Society",
number = "12",

}

TY - JOUR

T1 - Airway basal cells

T2 - The "smoking gun" of chronic obstructive pulmonary disease

AU - Crystal, Ronald

PY - 2014/1/1

Y1 - 2014/1/1

N2 - The earliest abnormality in the lung associated with smoking is hyperplasia of airway basal cells, the stem/progenitor cells of the ciliated and secretory cells that are central to pulmonary host defense. Using cell biology and 'omics technologies to assess basal cells isolated from bronchoscopic brushings of nonsmokers, smokers, and smokers with chronic obstructive pulmonary disease (COPD), compelling evidence has been provided in support of the concept that airway basal cells are central to the pathogenesis of smoking-associated lung diseases. When confronted by the chronic stress of smoking, airway basal cells become disorderly, regress to a more primitive state, behave as dictated by their inheritance, are susceptible to acquired changes in their genome, lose the capacity to regenerate the epithelium, are responsible for the major changes in the airway that characterize COPD, and, with persistent stress, can undergo malignant transformation. Together, these observations led to the conclusion that accelerated loss of lung function in susceptible individuals begins with disordered airway basal cell biology (i.e., that airway basal cells are the "smoking gun" of COPD, a potential target for the development of therapies to prevent smoking-related lung disorders).

AB - The earliest abnormality in the lung associated with smoking is hyperplasia of airway basal cells, the stem/progenitor cells of the ciliated and secretory cells that are central to pulmonary host defense. Using cell biology and 'omics technologies to assess basal cells isolated from bronchoscopic brushings of nonsmokers, smokers, and smokers with chronic obstructive pulmonary disease (COPD), compelling evidence has been provided in support of the concept that airway basal cells are central to the pathogenesis of smoking-associated lung diseases. When confronted by the chronic stress of smoking, airway basal cells become disorderly, regress to a more primitive state, behave as dictated by their inheritance, are susceptible to acquired changes in their genome, lose the capacity to regenerate the epithelium, are responsible for the major changes in the airway that characterize COPD, and, with persistent stress, can undergo malignant transformation. Together, these observations led to the conclusion that accelerated loss of lung function in susceptible individuals begins with disordered airway basal cell biology (i.e., that airway basal cells are the "smoking gun" of COPD, a potential target for the development of therapies to prevent smoking-related lung disorders).

KW - Airway epithelium

KW - Basal cells

KW - COPD

KW - Lung cancer

KW - Smoking

UR - http://www.scopus.com/inward/record.url?scp=84919399548&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84919399548&partnerID=8YFLogxK

U2 - 10.1164/rccm.201408-1492PP

DO - 10.1164/rccm.201408-1492PP

M3 - Review article

C2 - 25354273

AN - SCOPUS:84919399548

VL - 190

SP - 1355

EP - 1362

JO - American Journal of Respiratory and Critical Care Medicine

JF - American Journal of Respiratory and Critical Care Medicine

SN - 1073-449X

IS - 12

ER -