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Airway bacteria drive a progressive COPD-like phenotype in mice with polymeric immunoglobulin receptor deficiency

Bradley W Richmond1,2, Robert M Brucker3, Wei Han1

  • 1Division of Allergy, Pulmonary and Critical Care Medicine, Department of Medicine, Vanderbilt University School of Medicine, T-1218 MCN, Nashville, Tennessee 37232-2650, USA.

Nature Communications
|April 6, 2016
PubMed

Insights

Secretory IgA (SIgA) deficiency in airways causes chronic obstructive pulmonary disease (COPD)-like pathology in mice. Restoring SIgA or using anti-inflammatory drugs prevents this progression.

Area of Science:

  • Pulmonary Medicine
  • Immunology
  • Microbiology

Background:

  • Mechanisms of persistent airway inflammation in chronic obstructive pulmonary disease (COPD) remain unclear.
  • Secretory immunoglobulin A (SIgA) deficiency in small airways is observed in COPD patients.
  • Reduced SIgA may impair immunobarrier function, contributing to COPD.

Purpose of the Study:

  • To investigate the role of SIgA deficiency in the development of COPD-like pathology.
  • To determine if impaired immunobarrier function drives chronic airway inflammation and disease progression.

Main Methods:

  • Utilized polymeric immunoglobulin receptor-deficient (pIgR(-/-)) mice lacking SIgA to model disease.
  • Analyzed airway remodelling, emphysema, lung microbiome, and immune responses.
  • Assessed the effects of germ-free conditions and roflumilast treatment.

Main Results:

  • pIgR(-/-) mice spontaneously developed COPD-like pathology with aging.
  • Pathology included airway remodelling, emphysema, altered microbiome, bacterial invasion, and inflammation.
  • Germ-free conditions or roflumilast treatment prevented inflammation and remodelling.

Conclusions:

  • Airway pIgR/SIgA deficiency leads to persistent innate immune activation against lung microbiota.
  • This immune response drives progressive small airway remodelling and emphysema in COPD.
  • SIgA plays a critical role in maintaining airway homeostasis and preventing COPD progression.

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