In order to better understand how CI might drive frailty and the associated adverse outcomes, a mouse that is missing the gene that produces the anti-inflammatory cytokine interleukin 10 (IL-10) has been extensively studied as a model of frailty. This mouse gradually develops inflammatory pathway activation in early life, and like frail, older adults evolves skeletal muscle weakness and early mortality compared to age and gender matched control mice (Walston et al., 2008). With increasing age it also develops many of the signs and symptoms of frail, older adults including chronic anemia and metabolic and endocrine abnormalities (Ko et al., 2012; and Westbrook et al., 2017). Molecular studies in this mouse with CI have identified potential roles for altered cell death pathways, mitochondrial function, and lower mitochondrial energy production as possible drivers of the phenotype (Akki et al., 2014; Abadir et al., 2017; Sikka et al., 2012; and Ko et al., 2016).
Frailty is also known to be associated with many chronic disease states, including cardiovascular and pulmonary conditions (Newman et al, 2001). Because the biology that underlies physical frailty is also postulated to underlie the development and propogation of many chronic disease states some investigators have also used this mouse model of chronic inflammation and frailty to identify relationships between CI and chronic pulmonary and cardiovascular disease states (Calvi et al., 2011).