Molecular connections between inflammation and social determinants of health.

IF 2.9
Frontiers in epidemiology Pub Date : 2025-11-11 eCollection Date: 2025-01-01 DOI:10.3389/fepid.2025.1683955
Aditi Vijendra, Claire Kunkle, Jalin Jordan, Anna Erickson, Kingsley Osei-Karikari, Grace Ratley, Ian A Myles
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Abstract

Chronic inflammatory diseases such as autoimmune disorders, cancer, cardiovascular diseases and neurodegenerative disorders are a significant cause of morbidity and mortality in the industrialized world. Socioeconomically disadvantaged communities bear a disproportionately high burden of these inflammatory diseases. This review synthesizes evidence linking various domains of the Social Determinants of Health (SDoH)-economic stability, education access and quality, healthcare access and quality, neighborhood and built environment, and social and community context-to inflammatory pathways and mechanisms. Across domains, biological mechanisms such as cytokine dysregulation, toll-like receptor (TLR) activation, hypothalamic-pituitary-adrenal (HPA) axis alterations and gut microbiome disruption act together to sustain proinflammatory states that drive adverse health outcomes in marginalized communities. Although causality is obscured by interrelated determinants, identifying inflammation as a shared pathway between various determinants highlights the need for structural interventions to reduce chronic disease burden.

Abstract Image

Abstract Image

炎症与健康的社会决定因素之间的分子联系。
慢性炎症性疾病,如自身免疫性疾病、癌症、心血管疾病和神经退行性疾病,是工业化世界发病率和死亡率的重要原因。社会经济上处于不利地位的社区承受着这些炎症性疾病的不成比例的高负担。本综述综合了将健康的社会决定因素(SDoH)的各个领域——经济稳定性、教育机会和质量、医疗机会和质量、邻里和建成环境、社会和社区环境——与炎症途径和机制联系起来的证据。在各个领域,细胞因子失调、toll样受体(TLR)激活、下丘脑-垂体-肾上腺(HPA)轴改变和肠道微生物群破坏等生物机制共同作用,维持促炎状态,从而导致边缘化社区的不良健康结果。尽管因果关系被相互关联的决定因素所掩盖,但将炎症确定为各种决定因素之间的共享途径,强调了采取结构性干预措施以减轻慢性疾病负担的必要性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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