ArticleFrontiers in immunology2026
Cross-talk between lipopolysaccharide tolerance and AGEs in the regulation of macrophage inflammation and cholesterol efflux.
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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1 citing paper in PubMed.
- RORα: a critical nexus in the crosstalk between cholesterol metabolism and macrophage polarization.Frontiers in immunology · 2026Review
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11 authors.
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Abstract
Introduction: Immune cell infiltration with high expression of receptors for advanced glycation end products (RAGE) and Toll-like receptor 4 (TLR4) promotes vascular inflammation and accelerates atherosclerosis. Advanced glycated albumin (AGE-albumin) primes macrophages for heightened inflammatory responses to lipopolysaccharide (LPS). Here, we investigated whether LPS-induced tolerance modulates AGE-driven inflammatory priming and cholesterol efflux in macrophages. Methods: Cholesterol-enriched bone marrow-derived macrophages (BMDMs) and RAW264.7 macrophages were subjected to LPS tolerance induction, treated with control (C)- or AGE-albumin, and rechallenged with LPS. In parallel, LPS tolerance was induced Results: In BMDMs, LPS tolerance reduced TNF secretion following C-albumin treatment but not AGE-albumin. In RAW264.7 macrophages, TNF secretion was reduced by 53% and 77.6% after C- and AGE-albumin treatment, respectively. BMDMs from LPS-tolerant mice exhibited reduced TNF secretion following both albumin treatments. Gene expression analysis revealed that AGE-albumin selectively increased Discussion: These findings demonstrate that LPS tolerance promotes an atheroprotective macrophage phenotype characterized by attenuated inflammatory signaling and enhanced cholesterol efflux. However, this protective immunometabolic program is selectively disrupted by AGE exposure, highlighting a critical interface through which chronic metabolic stress may override innate immune tolerance and contribute to atherosclerotic progression.
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