Thoracic adipose tissue contributes to severe virus infection of the lung
Authors' conclusion
Our study revealed that thoracic adipose tissue contributes to respiratory virus infection. Besides indirect induction of proinflammatory factors during infection, adipocytes and macrophages within the tissue can directly support viral replication.
Study context
- Population
- Two murine obesity models infected with IAV and monitored 3 weeks p.i.; human derived primary adipocytes and macrophages in vitro; lung and adipose tissue from deceased patients infected with SARS-CoV-2 omicron variant
- Comparison
- Obese vs non-obese mice infected with IAV; viral replication in adipocytes and macrophages in vitro
- Outcome
- Viral load in lung and adipose tissue, and direct viral replication in adipocytes and macrophages
- Follow-up
- 3 weeks p.i.
Methodological detailsmurine obesity models, in vitro human primary adipocytes and macrophages, adipocyte–lung fibroblast co-culture, post-mortem human lung and adipose tissue
- Murine obesity models
- In vitro human primary adipocytes and macrophages
- Adipocyte–lung fibroblast co-culture
- Post-mortem human lung and adipose tissue
Main finding
As reported in the abstract
IAV and SARS-CoV-2 in thoracic adipose tissue and in adipocytes/macrophages
- High IAV titres in both murine obesity models vs non-obese mice
- Adipose tissue adjacent to the lungs a focal point for IAV replication in mice
- IAV replication and antiviral response detected in human adipocytes
- SARS-CoV-2 observed in thoracic adipose tissue of COVID-19 patients, but no active replication in adipocytes in vitro
- SARS-CoV-2 detected in macrophages, associated with increased inflammation
- SARS-CoV-2 alpha, delta and omicron variants tested in vitro
Further findings
IL-8 concentration in adipocyte–lung fibroblast co-culture
- Increased IL-8 concentration during infection on co-cultivation of adipocytes and lung fibroblasts
Original publication
Thoracic adipose tissue contributes to severe virus infection of the lung. Int J Obes (Lond). Published 16 August 2023. doi:10.
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