Figure 1
- Alveoli are part of the lungs
- CO2 goes into the alveoli and oxygen leaves the alveoli and enters the pulmonary vein
- Due to COVID-19, immune cells are activated in the alveoli
- Epithelial cells become infected
- Inflammation is prevented
- Cytokine and chemokine are released into the pulmonary vein
- However, a cytokine storm indicates severe cases of COVID-19
- In severe cases of COVID-19, inflammation occurs → ARDS, organ failure, etc.


Michigan State University

Smith College

A main feature of symptomatic COVID-19 disease is respiratory infection. Severe damage to the lungs during respiratory distress may cause pulmonary fibrosis, necessitating lung transplants. Lasting damages to the lungs may occur even in recovering patients with mild infections. SARS-CoV-2 targets the following cell types:

- Type I pneumocytes (AT1) 
- Type II pneumocytes (AT2) 
- alveolar macrophages

ACE2 expression is primarily seen in AT2 cells which have been shown to be involved in the reproduction and transmission of the virus.  Viral targeting of alveolar macrophages is evidenced by N antigen expression.

Effects of COVID-19 on the Lungs

Solinas, C., Perra, L., Aiello, M., Migliori, E., & Petrosillo, N. (2020). A critical evaluation of glucocorticoids in the treatment of severe COVID-19. Cytokine & Growth Factor Reviews. doi: 10.1016/j.cytogfr.2020.06.012 https://pubmed.ncbi.nlm.nih.gov/32616381/

A critical evaluation of glucocorticoids in the management of severe COVID-19

Pulmonary Alveoli and its Physiology in Relation to COVID-19

- Pulmonary fibrosis has been found in the autopsies of severe COVID-19 patients
- It is possible that the cytokine storm can result in pulmonary fibrosis
- Antifibrotic therapy can be useful in identifying COVID-19 patients that are on the verge of developing pulmonary fibrosis
- Nintedanib therapy prevents to formation of fibrinogen in the lungs (pirfenidone could potentially have the same effects)
- IPF results in damage to alveoli in the lungs


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