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Chronic Obstructive Pulmonary Disease-II: Pathophysiology01:20

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Chronic Obstructive Pulmonary Disease (COPD) pathophysiology is intricate and multifaceted, involving a complex interplay of physiological processes. Understanding these mechanisms is crucial for effectively managing and treating COPD. Here is an in-depth look at the critical elements in the pathophysiology of COPD:
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Cigarette Smoke Exposure in Mice using a Whole-Body Inhalation System
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Cigarette Smoke Deteriorates SARS-CoV-2 Infection-Induced Lung Injury.

Rui Chen1,2, Kenrie P Y Hui2,3, John M Nicholls4

  • 1Department of Medicine, School of Clinical Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, China.

Journal of Medical Virology
|October 30, 2025
PubMed
Summary
This summary is machine-generated.

Cigarette smoke (CS) exposure worsens COVID-19 severity by increasing viral susceptibility and endoplasmic reticulum (ER) stress. This leads to greater lung damage and immune response in smokers infected with SARS-CoV-2.

Keywords:
COPDCOVID‐19SARS‐CoV‐2cigarette smokingendoplasmic reticulum stress

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Area of Science:

  • Pulmonary Medicine
  • Virology
  • Toxicology

Background:

  • COVID-19, caused by SARS-CoV-2, is a global pandemic.
  • COPD, often linked to CS, is a risk factor for severe COVID-19.
  • Understanding host-viral interactions in smokers is crucial.

Purpose of the Study:

  • To investigate the impact of CS exposure on SARS-CoV-2 susceptibility and disease severity.
  • To elucidate the role of ER stress in CS-exacerbated COVID-19 lung injury.

Main Methods:

  • K18-hACE2 transgenic mice were exposed to CS or sham air.
  • Mice were subsequently infected with SARS-CoV-2 or mock.
  • Lung tissues were analyzed for viral load, ER stress markers, immune response, and histopathology.

Main Results:

  • CS exposure upregulated ACE2 and BiP, increasing viral susceptibility.
  • CS induced ER stress via ATF6 and PKR pathways, promoting apoptosis.
  • Prior CS exposure exacerbated SARS-CoV-2-induced epithelial damage, ciliary dysfunction, and lung fibrosis.

Conclusions:

  • ER stress plays a significant role in CS-exacerbated SARS-CoV-2 lung injury.
  • CS exposure worsens COVID-19 pathogenesis in smokers.
  • Findings suggest potential therapeutic targets for treating smokers with COVID-19.