SARS-CoV-2 (COVID-19) Adhesion Site Protein Upregulation in Small Airways, Type 2 Pneumocytes, and Alveolar Macrophages of Smokers and COPD - Possible Implications for Interstitial Fibrosis.
Samuel James BrakeMathew Suji EapenKielan Darcy McAlindenJames MarkosGreg HaugJosie LarbyCollin ChiaAshutosh HardikarGurpreet Kaur SingheraTillie L HackettWenying LuSukhwinder Singh SohalPublished in: International journal of chronic obstructive pulmonary disease (2022)
The increased expression of ACE2, TMPRSS2 and Furin, in the SAE, type 2 pneumocytes and AMs of smokers and COPD are detrimental to lung function and proves that these patient groups could be more susceptible to severe COVID-19 infection. Increased type 2 pneumocytes suggest that these patients are vulnerable to developing post-COVID-19 interstitial pulmonary fibrosis or fibrosis in general. There could be a silently developing interstitial pathology in smokers and patients with COPD. This is the first comprehensive study to report such changes.
Keyphrases
- lung function
- sars cov
- chronic obstructive pulmonary disease
- cystic fibrosis
- air pollution
- coronavirus disease
- smoking cessation
- pulmonary fibrosis
- poor prognosis
- end stage renal disease
- respiratory syndrome coronavirus
- ejection fraction
- chronic kidney disease
- newly diagnosed
- pseudomonas aeruginosa
- signaling pathway
- cell proliferation
- escherichia coli
- staphylococcus aureus
- patient reported
- liver fibrosis
- protein protein
- cell migration