ATS 2021 will feature presentations of original research from accepted abstracts. Mini Symposia and Thematic Poster Sessions are abstract based sessions.
Please use the form below to browse scientific abstracts and case reports accepted for ATS 2021. Abstracts presented at the ATS 2021 will be published in the Online Abstract Issue of the American Journal of Respiratory and Critical Care Medicine, Volume 203, May 3, 2021.
Search Tips:
- Use the keyword search to search by keyword or author's name.
- Filter your search results by selecting the checkboxes that apply.
- Click on "Clear" to clear the form and start a new search. .
Search results will display below the form.
SARS-CoV-2-Related Gene Expression in Alveolar Type II Cells in Aging and Emphysema
Session Title
TP105 - TP105 BASIC MECHANISMS OF LUNG INFECTIONS: FROM SARS-COV-2 TO INFLUENZA
Abstract
A4192 - SARS-CoV-2-Related Gene Expression in Alveolar Type II Cells in Aging and Emphysema
Author Block: B. Kosmider1, C. Lin1, H. Simborio1, S. Bolla1, N. Marchetti2, G. J. Criner3, K. Bahmed1; 1Thoracic Medicine and Surgery, Temple University, Philadelphia, PA, United States, 2Pulmonary Division, Temple University Hospital, Philadelphia, PA, United States, 3Pulmonary & Critical Care Medicine, Temple University Hospital, Philadelphia, PA, United States.
RATIONALE: The alveolar epithelium is the barrier between inhaled air and the underlying tissue. Alveolar type II (ATII) cells produce and secrete pulmonary surfactant and restore the injured epithelium. It has been reported that SARS-CoV-2 infection causes diffused alveolar damage in the lung. However, host factors facilitating virus infection and COVID-19 pathogenesis are not well known. METHODS: We isolated ATII cells from young and elderly non-smoker, smoker, and ex-smoker organ donors. Also, cells were obtained from lung transplants of emphysema patients. Gene and protein expression related to SARS-CoV-2 infection were analyzed using RT-PCR and Western blotting, respectively. RESULTS: ACE2 was identified as a receptor mediating infection. We found that its levels were significantly increased in ATII cells isolated from elderly smokers compared to non-smokers as detected by Western blotting. ACE2 expression was also higher in ATII cells obtained from emphysema patients compared to non-smokers. ACE2 mRNA levels were increased in elderly non-smokers and smokers compared to young organ donors regardless of smoking status. The viral entry depends on TMPRSS2 protease activity. We detected its increased levels in elderly smokers than young non-smokers by Western blotting. Both ACE2 and TMPRSS2 mRNA levels were higher in emphysema in comparison with non-smokers. Moreover, we found increased CD209L gene and protein levels in young smokers and emphysema patients compared to non-smokers. Furthermore, GRP78, an endoplasmic reticulum chaperone, is an important host factor for viral infection. We detected its increased expression in ATII cells isolated from young and elderly smokers compared to non-smokers by Western blotting. Also, its higher levels were observed in emphysema patients than in non-smokers. CONCLUSION: Our results suggest dysregulation of SARS-CoV-2 infection-related genes and proteins especially in elderly smokers and emphysema patients, which may provide insight into the pathogenesis of COVID-19.
Author Block: B. Kosmider1, C. Lin1, H. Simborio1, S. Bolla1, N. Marchetti2, G. J. Criner3, K. Bahmed1; 1Thoracic Medicine and Surgery, Temple University, Philadelphia, PA, United States, 2Pulmonary Division, Temple University Hospital, Philadelphia, PA, United States, 3Pulmonary & Critical Care Medicine, Temple University Hospital, Philadelphia, PA, United States.
RATIONALE: The alveolar epithelium is the barrier between inhaled air and the underlying tissue. Alveolar type II (ATII) cells produce and secrete pulmonary surfactant and restore the injured epithelium. It has been reported that SARS-CoV-2 infection causes diffused alveolar damage in the lung. However, host factors facilitating virus infection and COVID-19 pathogenesis are not well known. METHODS: We isolated ATII cells from young and elderly non-smoker, smoker, and ex-smoker organ donors. Also, cells were obtained from lung transplants of emphysema patients. Gene and protein expression related to SARS-CoV-2 infection were analyzed using RT-PCR and Western blotting, respectively. RESULTS: ACE2 was identified as a receptor mediating infection. We found that its levels were significantly increased in ATII cells isolated from elderly smokers compared to non-smokers as detected by Western blotting. ACE2 expression was also higher in ATII cells obtained from emphysema patients compared to non-smokers. ACE2 mRNA levels were increased in elderly non-smokers and smokers compared to young organ donors regardless of smoking status. The viral entry depends on TMPRSS2 protease activity. We detected its increased levels in elderly smokers than young non-smokers by Western blotting. Both ACE2 and TMPRSS2 mRNA levels were higher in emphysema in comparison with non-smokers. Moreover, we found increased CD209L gene and protein levels in young smokers and emphysema patients compared to non-smokers. Furthermore, GRP78, an endoplasmic reticulum chaperone, is an important host factor for viral infection. We detected its increased expression in ATII cells isolated from young and elderly smokers compared to non-smokers by Western blotting. Also, its higher levels were observed in emphysema patients than in non-smokers. CONCLUSION: Our results suggest dysregulation of SARS-CoV-2 infection-related genes and proteins especially in elderly smokers and emphysema patients, which may provide insight into the pathogenesis of COVID-19.
