As the body ages, subtle changes in immune function can fuel persistent, low-grade inflammation, a phenomenon scientists call “inflammaging.” This process is increasingly recognised as a contributor to cardiovascular disease, neurodegeneration, metabolic disorders and physical frailty in older adults.
Inflammaging develops through several interconnected mechanisms. Immunosenescence, the age-related decline in immune function, impairs the body’s ability to clear damaged or senescent cells. Meanwhile, telomere shortening, mitochondrial dysfunction and oxidative stress promote cellular damage. These damaged cells release molecules that activate inflammatory pathways, creating a self-reinforcing cycle.
At the molecular level, inflammaging involves dysregulated signalling of inflammatory markers including interleukin-6, IL-1β and tumour necrosis factor-alpha. Senescent cells that resist normal programmed cell death produce what scientists term the senescence-associated secretory phenotype (SASP), which includes inflammatory cytokines that can damage surrounding healthy tissues.
The gut microbiome also plays a role. Ageing can alter microbial composition and diversity, potentially impairing intestinal barrier function. When microbial products cross this barrier, they can stimulate immune receptors and sustain systemic inflammation.
Lifestyle factors offer non-pharmacological approaches to reducing chronic inflammation. Regular physical activity can lower resting C-reactive protein and TNF-α levels, whilst diets rich in fibre and plant-based foods support gut microbial health and immune regulation.
Emerging research is investigating pharmacological interventions, including senolytics that selectively clear senescent cells. However, evidence for their benefits in preventing age-related disease in humans remains limited. Any intervention must balance reducing persistent inflammation with preserving immune responses needed for pathogen clearance and tissue repair.
Source: News Medical overview article drawing on multiple peer-reviewed sources including Teissier T et al. Cells (2022); Furman D et al. Nature Medicine (2019); Ferrucci L & Fabbri E. Nature Reviews Cardiology (2018).
