A role of stimulator of interferon genes (STING) signaling in obesity-induced lung inflammation
Authors' conclusion
Our results collectively suggest that the STING signaling contributes to obesity-associated inflammation by stimulating proinflammatory processes in lung macrophages, one that may serve as a therapeutic target in ameliorating obesity-related lung dysfunctions.
Study context
- Population
- Human lung tissues from obese patients and controls; Diet-induced obese (DIO) and lean mice; lung macrophages exposed to palmitic acid in vitro
- Comparison
- Obesity vs controls; STING inhibitor C-176 vs vehicle
- Obesen = 3
- Controlsn = 3reference
- Outcome
- STING signaling and lung inflammation in obesity
Methodological detailshuman lung tissue, diet-induced obese mouse model, in vitro macrophage experiments
- Human lung tissue
- Diet-induced obese mouse model
- In vitro macrophage experiments
Main finding
As reported in the abstract
- STING+/CD68+ macrophages increased in lung tissues of patients with obesity
- STING expression and proinflammatory cytokines increased in lung tissues and bronchoalveolar lavage fluid (BALF) in obesity vs controls
- STING inhibition blunted obesity-induced lung inflammation
- STING involved in palmitic acid-induced inflammation via STING-TBK1-IRF3/NF-κB pathways in lung macrophages
Original publication
A role of STING signaling in obesity-induced lung inflammation. Int J Obes (Lond). Published 13 February 2023. doi:10.
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