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  3. A role of STING signaling in obesity-induced lung inflammation

A role of STING signaling in obesity-induced lung inflammation

  • Int J Obes (Lond). 2023 Feb 13;1-10. doi: 10.1038/s41366-023-01272-x.
Yong Qi # 1,  Zhuhua Wu # 2,  Dan Chen 2 3,  Li Zhu 2,  Yunlei Yang 4 5 6 7
Affiliations

Affiliations

  • 1 Department of Pulmonary and Critical Care Medicine, Zhengzhou University People's Hospital, Henan Provincial People's Hospital, Zhengzhou, Henan, 450003, China. qiyong@zzu.edu.cn.
  • 2 Department of Pulmonary and Critical Care Medicine, Zhengzhou University People's Hospital, Henan Provincial People's Hospital, Zhengzhou, Henan, 450003, China.
  • 3 Department of Medicine Division of Endocrinology, Albert Einstein College of Medicine, Bronx, NY, 10461, USA.
  • 4 Department of Medicine Division of Endocrinology, Albert Einstein College of Medicine, Bronx, NY, 10461, USA. yunlei.yang@einsteinmed.edu.
  • 5 Department of Neuroscience, Albert Einstein College of Medicine, Bronx, NY, 10461, USA. yunlei.yang@einsteinmed.edu.
  • 6 Einstein-Mount Sinai Diabetes Research Center, Albert Einstein College of Medicine, Bronx, NY, 10461, USA. yunlei.yang@einsteinmed.edu.
  • 7 The Fleischer Institute for Diabetes and Metabolism, Albert Einstein College of Medicine, Bronx, NY, 10461, USA. yunlei.yang@einsteinmed.edu.
  • # Contributed equally.
PMID: 36782056 DOI: 10.1038/s41366-023-01272-x
Abstract

Background: It is established that pulmonary disorders are comorbid with metabolic disorders such as obesity. Previous studies show that the stimulator of interferon genes (STING) signaling plays crucial roles in obesity-induced chronic inflammation via TANK-binding kinase 1 (TBK1) pathways. However, it remains unknown whether and how the STING signaling is implicated in the inflammatory processes in the lung in obesity.

Methods: Human lung tissues were obtained from obese patients (n = 3) and controls (n = 3). Mice were fed with the high-fat diet or regular control diet to establish the diet-induced obese (DIO) and lean mice, and were treated with C-176 (a specific STING Inhibitor) or vehicle respectively. The lung macrophages were exposed to palmitic acid (PA) in vitro. The levels of STING singaling and metabolic inflammation factors were detected and anlyzed.

Results: We find that STING+/CD68+ macrophages are increased in lung tissues in patients with obesity. Our data also show that the expressions of STING and the levels of proinflammatory cytokines are increased both in lung tissues and bronchoalveolar lavage fluid (BALF) in obesity compared to controls, and inhibition of the STING blunted the obesity-induced lung inflammation. Mechanistically, our data demonstrate that the STING signaling pathway is involved in the PA-induced inflammation through the STING-TBK1-IRF3 (interferon regulatory factor 3)/NF-κB (nuclear factor kappa B) pathways in the lung macrophages.

Conclusions: 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.

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