ArticleFrontiers in immunology2026
Obesity and COVID-19 severity independently shape adipokine dysregulation and immune cell remodeling.
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Obesity is a major risk factor for severe COVID-19, yet the immunological mechanisms by which it modifies disease progression remain incompletely characterized. We aimed to dissect the independent and interactive contributions of obesity and COVID-19 severity on circulating adipokines, cytokines, and immune cell populations. Methods: Sixty patients with confirmed SARS-CoV-2 infection were stratified by disease severity (Mild/Moderate, n = 8; Severe, n = 30; Critical, n = 22) and obesity status (persons without obesity [PwoO], n = 30; persons with obesity [PwO], n = 30; BMI threshold 30 kg/m²). Serum TNF-α, resistin, IL-1β, IL-8, and NETs-ISG15 complexes were measured alongside circulating Th1, Th2, Th17, CD8 Treg, CD8 Tcm, intermediate monocytes, and low-density granulocytes (LDGs). Statistical analysis used Aligned Rank Transform ANOVA (ART-ANOVA), followed by Kruskal-Wallis and Dunn's Results: ART-ANOVA identified three distinct immunological patterns. First, TNF-α and resistin were significantly elevated by obesity as independent main effects (p = 0.012 and p = 0.026), with resistin additionally driven by severity (p = 0.0001). Second, IL-1β, IL-8, and NETs-ISG15 complexes were governed by disease severity (p = 0.0003, p = 0.0003, p = 0.002); IL-1β showed a symmetric Severe-to-Critical elevation across obesity strata, whereas IL-8 and NETs-ISG15 were selectively amplified in PwO at the critical stage (Severe vs. Critical: IL-8 p = 0.0002; NETs-ISG15 p = 0.015). Third, CD8 Treg cells and LDGs showed the largest severity-driven effects (both p < 0.0001), with symmetric depletion and expansion across obesity strata, identifying them as severity biomarkers independent of metabolic background. Th17 cells were suppressed by obesity (p = 0.001) and severity (p = 0.021). CD8 Tcm exhibited a unique obesity × severity interaction (p = 0.009), with a paradoxical expansion in critical PwO patients, absent in PwoO. Conclusion: Obesity and COVID-19 severity exert distinct, non-interacting effects on the immune landscape, with three exceptions: TNF-α and IL-8/NETs-ISG15 show obesity-conditional amplification of severity, and CD8 Tcm undergoes an obesity-specific expansion at the critical stage. These findings provide a mechanistic framework for obesity-modified immune responses in COVID-19 and identify candidate biomarkers for severity stratification.
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