Can inflammation regulate systemic aging?

Senescence, at both the cellular and organismal levels, results from an accumulation of genetic and epigenetic changes that lead to progressive cell deterioration, impaired tissue function, homeostatic imbalance, declining resilience in response to stressors, and a subsequent vulnerability to age-induced disease development (Burton, 2009). While a single mechanism for the cause and progression of biological aging has not been established, among the most common theories include telomere attrition, endocrine disorders, and oxidative stress (Kirkwood, 1988). Despite these widely accepted models, however, the etiology of senescence at the cellular and molecular levels remains largely undefined. Previous studies have suggested that chronic inflammation contributes to cellular senescence by propelling basic aging processes (Ren et al., 2009).While the immune response characteristic of acute inflammation dampens within days, chronic inflammation is characterized by elevated levels of pro-inflammatory cytokines in response to physiological and environmental stressors that essentially arrest the immune system in a state of low-level activation (Baylis et al., 2013). The chronically active immune system associated with advancing age, termed “inflammaging,” eventually initiates immunosenescence, the functional decline of the immune system with age (Franceschi et al., 2007; Freund et al., 2010). Although definitive mechanisms are yet to be identified, the pro-inflammatory phenotype of senescent cells, coupled with the up-regulation of the inflammatory responsewith increasing age, has been found to play a role in the initiation and progression of age-