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Related Concept Videos

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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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α5 Nicotinic Receptor Polymorphism affects cigarette smoke-induced inflammation and COPD development.

Layal Massara1,2, Lynda Saber Cherif3, Anais Ollivier1

  • 1Univ. Lille, CNRS, INSERM, CHU Lille, Institut Pasteur de Lille, U1019-UMR 9017, Center for Infection and Immunity of Lille, Lille, France.

American Journal of Respiratory Cell and Molecular Biology
|May 4, 2026
PubMed
Summary

The alpha-5 nicotinic acetylcholine receptor polymorphism (α5SNP) increases susceptibility to COPD in smokers. This genetic marker is prevalent in COPD patients and linked to heightened inflammation, emphasizing its role in disease development.

Keywords:
1. Pulmonary Disease, Chronic Obstructive/genetics2. Gene-Environment Interaction3. Receptors, Nicotinic/genetics4. Inflammation Mediators

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Area of Science:

  • Respiratory Medicine
  • Genetics
  • Immunology

Background:

  • Chronic Obstructive Pulmonary Disease (COPD) is a leading global cause of death, with cigarette smoke being the primary risk factor.
  • Genetic susceptibility plays a crucial role, as only a subset of smokers develop COPD.
  • The alpha-5 nicotinic acetylcholine receptor polymorphism (α5SNP; rs16969968) is implicated in immune responses to cigarette smoke and is found in most COPD patients.

Purpose of the Study:

  • To investigate the influence of α5SNP on cigarette smoke-induced inflammation and COPD pathogenesis.
  • To evaluate the role of α5SNP in both experimental models and human COPD cohorts.

Main Methods:

  • A murine knock-in model with varying α5SNP alleles (WT, HE, HO) was exposed to cigarette smoke for 1-3 months.
  • Evaluated lung function, histopathology, immune cell profiling, and cytokine expression in mice.
  • Assessed α5SNP prevalence and cytokine concentrations in a human COPD cohort.

Main Results:

  • Cigarette smoke exposure worsened lung function across genotypes, with heterozygous (HE) mice showing the most severe airflow limitation, inflammation, and airway remodeling.
  • The observed phenotype in HE mice was associated with increased γδ T cell activation and TNF-α, linked to altered macrophage nAChR signaling.
  • In humans, α5SNP was highly prevalent in COPD patients and correlated with elevated systemic inflammation.

Conclusions:

  • The α5SNP genetic variant enhances susceptibility to cigarette smoke-induced lung injury.
  • α5SNP is a significant genetic marker for COPD susceptibility and is present in the majority of affected patients.
  • Identifying α5SNP in smokers warrants precise follow-up due to increased COPD risk.