ArticleObesity (Silver Spring, Md.)2024
Adipocyte-derived inflammatory molecules induce senescent B cells through metabolic pathways.
Article in Obesity (Silver Spring, Md.), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 5 citations in OpenAlex.
- Low-dose tamoxifen ameliorates ovariectomy-induced metabolic and immune dysfunction.GeroScience · 2026Article
- Cancer-associated adipocytes: metabolic reprogramming, crosstalk and therapeutic implications in tumor progression.Signal transduction and targeted therapy · 2026Review
- Immune cell senescence in autoimmunity: implications for disease pathogenesis and therapeutic targeting.Frontiers in immunology · 2025Review
- The infection-microbiome-immunity axis in bladder cancer: mechanistic insights and therapeutic perspectives.Frontiers in immunology · 2025Review
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
objectiveThe aim of this study was to demonstrate that an adipocyte tissue-derived conditioned medium (ACM) contains inflammatory molecules that induce senescence in B cells.
methodsWe incubated blood-derived B cells from lean donors with ACM obtained from the adipose tissue of adult female donors with obesity undergoing weight reduction surgery or with medium as control. After 24 h, cells were harvested, and the expression of transcripts for proinflammatory cytokines (TNF/IL-6), chemokines (IL-8), and for markers of the senescence-associated secretory phenotype (SASP) was measured by quantitative polymerase chain reaction. B cells were also stained with the marker of immunosenescence β-galactosidase, and their metabolic status was evaluated in Seahorse using a Mito Stress Test.
resultsWe show that the incubation of B cells from lean donors with ACM induces the expression of transcripts for inflammatory and SASP transcripts, increases the amount of β-galactosidase staining, and induces a metabolic phenotype characterized by higher basal and maximal oxygen consumption, spare respiratory capacity (difference between maximal and basal respiration), nonmitochondrial oxygen consumption, ATP production, and proton leak.
conclusionsThese results demonstrate that B cells from lean individuals, after incubation with ACM, become inflammatory and senescent, and this occurs through metabolic pathways needed to support their secretory phenotype.
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Registered trials
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