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Updated: Aug 11, 2026
07:46
Isolation, Characterization, and Purification of Macrophages from Tissues Affected by Obesity-related Inflammation
Published on: April 3, 2017
Chronic Intermittent Hypoxia Promotes Macrophage Inflammation Through Reduction of Adipocyte‑Derived Adiponectin
Xiaoqin Weng1, Hengrui Zhang1, Mao Huang2
1Department of Respiratory and Critical Care Medicine, The Second Affiliated Hospital of Nanjing Medical University, Nanjing, 210000, People's Republic of China.
Journal of Inflammation Research
|August 10, 2026
Summary
Chronic intermittent hypoxia (CIH) promotes macrophage inflammation through adipocyte signaling. Adiponectin (Ad) can mitigate this inflammation, suggesting a therapeutic target for metabolic disorders.
Area of Science:
- Metabolic disorders
- Adipose tissue biology
- Inflammation research
Background:
- Macrophage inflammation in adipose tissue is linked to metabolic disorders caused by chronic intermittent hypoxia (CIH).
- The precise mechanisms driving this inflammation are not fully understood.
- Adiponectin (Ad), an adipocyte-secreted adipokine, is vital for insulin sensitivity.
Purpose of the Study:
- To investigate if adipocyte-derived paracrine signals mediate CIH-induced macrophage inflammation.
- To determine if Ad can attenuate CIH-induced macrophage inflammation.
Main Methods:
- Utilized a co-culture system involving iBMDM macrophages and 3T3-L1 adipocytes (direct and indirect).
- Exposed co-cultures to CIH and Ad treatment.
- Quantified inflammatory factor levels in conditioned media.
Main Results:
- CIH alone did not induce inflammation in isolated macrophages or adipocytes.
- CIH significantly increased inflammatory factor release in co-cultured cells.
- Adiponectin (Ad) reduced the pro-inflammatory effects of adipocytes on macrophages under CIH.
Conclusions:
- Chronic intermittent hypoxia (CIH) disrupts adipocyte function.
- Adipocyte-derived paracrine signals promote macrophage inflammation under CIH.
- Adiponectin (Ad) plays a protective role by attenuating this inflammation.
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