ArticleBMJ open diabetes research & care2019
Peritoneal macrophages have an impaired immune response in obesity which can be reversed by subsequent weight loss.
Article in BMJ open diabetes research & care, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 16 citations in OpenAlex.
- Masterful macrophages: understanding and targeting activation dysfunction in diabetic wounds.Burns & trauma · 2025Review
- Innate immune memory in cardiometabolic disease.Cardiovascular research · 2024Review
- The Influence of Obesity and Weight Loss on the Bioregulation of Innate/Inflammatory Responses: Macrophages and Immunometabolism.Nutrients · 2022Review
- Metabolic Regulation of Macrophage Activation.Journal of innate immunity · 2022Review
- Diet-induced obesity in mice impairs host defense againstAmerican journal of physiology. Lung cellular and molecular physiology · 2022Article
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
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Abstract
Introduction: Obesity is recognized as a risk factor for various microbial infections. The immune system, which is affected by obesity, plays an important role in the pathophysiology of these infections and other obesity-related comorbidities. Weight loss is considered the most obvious treatment for obesity. However, multiple studies suggest that the comorbidities of obesity may persist after weight loss. Deregulation of immune cells including adipose tissue macrophages of obese individuals has been extensively studied, but how obesity and subsequent weight loss affect immune cell function outside adipose tissue is not well defined. Research design and methods: Here we investigated the phenotype of non-adipose tissue macrophages by transcriptional characterization of thioglycollate-elicited peritoneal macrophages (PM) from mice with diet-induced obesity and type 2 diabetes (T2D). Subsequently, we defined the characteristics of PMs after weight loss and mimicked a bacterial infection by exposing PMs to lipopolysaccharide. Results and conclusions: In contrast to the proinflammatory phenotype of adipose tissue macrophages in obesity and T2D, we found a deactivated state of PMs in obesity and T2D. Weight loss could reverse this deactivated macrophage phenotype. Anti-inflammatory characteristics of these non-adipose macrophages may explain why patients with obesity and T2D have an impaired immune response against pathogens. Our data also suggest that losing weight restores macrophage function and thus contributes to the reduction of immune-related comorbidities in patients.
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