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Altered sphingolipid pathway in SARS-CoV-2 infected human lung tissue
Rabisa J Khan1,2, Sierra L Single1, Christopher S Simmons2
1Department of Medicine, Division of Pulmonary, Allergy, and Critical Care Medicine, University of Alabama at Birmingham, Birmingham, AL, United States.
Frontiers in Immunology
|October 23, 2023
Summary
COVID-19 infection alters lung tissue structure and sphingolipid metabolism. Sphingosine-kinase-1 (SK1) is upregulated, potentially contributing to inflammation and tissue damage in SARS-CoV-2 patients.
Area of Science:
- Pulmonary pathology
- Molecular biology
- Immunology
Background:
- The COVID-19 pandemic involves hyper-inflammatory processes and tissue injury.
- Sphingolipid metabolism, regulated by sphingosine-kinase-1 (SK1) and ceramide-synthase-2 (CERS2), influences inflammatory responses.
- Alterations in SK1 and CERS2 may contribute to COVID-19-related inflammation and damage.
Purpose of the Study:
- To evaluate lung structural changes after SARS-CoV-2 infection.
- To investigate alterations in the sphingolipid rheostat in response to SARS-CoV-2.
Main Methods:
- Histologic evaluation of lung autopsy and convalescent tissues for airspace and collagen deposition.
- Immunohistochemical analysis of SK1 and CERS2 expression in lung tissues.
Main Results:
- Significant reduction in airspace and increased collagen deposition were observed in COVID-19 lungs.
- Sphingosine-kinase-1 (SK1) expression was upregulated in COVID-19 lungs, particularly in Type II pneumocytes and alveolar macrophages.
- No significant change in ceramide-synthase-2 (CERS2) expression was detected; however, the SK1 to CERS2 ratio increased.
Conclusions:
- SARS-CoV-2 infection alters the sphingolipid rheostat in lung tissue.
- Upregulation of SK1 and the altered SK1/CERS2 ratio may contribute to COVID-19-associated lung inflammation and tissue damage.
