Age-Related Inflammation, or “inflammaging,” is the chronic, low-grade, systemic inflammatory state that progressively increases with chronological age. This pervasive condition is characterized by persistently elevated circulating levels of pro-inflammatory cytokines such as Interleukin-6 and Tumor Necrosis Factor-alpha. It is a sterile, non-infectious inflammation recognized as a fundamental, non-pathological driver of immunosenescence and a significant contributor to numerous age-associated chronic diseases. The continuous low-level inflammatory signal disrupts endocrine and metabolic homeostasis, accelerating biological decline.
Origin
The concept emerges from the convergence of immunology and gerontology, noting the consistent pro-inflammatory phenotype observed in aging individuals, independent of acute infection. The root cause is intrinsically linked to the cumulative burden of cellular senescence and the dysregulation of the innate immune system over decades. This process reflects a gradual loss of the body’s capacity to effectively resolve inflammatory events, leading to a persistent state of immunological stress. It highlights the systemic impact of cellular waste and immune system exhaustion on overall healthspan.
Mechanism
The mechanism is centered on the accumulation of senescent cells, which release the Senescence-Associated Secretory Phenotype (SASP), a potent mix of pro-inflammatory molecules. Concurrently, age-related decline in thymic function and a shift in macrophage polarization contribute to the persistent, low-level signal. This chronic cytokine release interferes with key endocrine signaling pathways, notably impairing insulin sensitivity and disrupting the delicate balance of the hypothalamic-pituitary-adrenal axis. The result is a positive feedback loop that accelerates tissue damage and functional decline.
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