Chronic inflammation increases with aging due to a progressive dysfunction of the immune system: it is overactive but yet ineffective, like a failing engine running hot. Inflammation is a necessary part of the immune response, but if it is turned on all the time it causes all sorts of secondary forms of damage, and is associated with an increased risk of developing many of the common forms of age-related disease. Thus many research groups are interested in finding effective ways to reduce inflammation in aging, either by addressing the root causes of immune dysfunction, or more commonly, and as is the case here, by trying to alter biochemical signals and responses to those root causes:
Aging is associated with an overt inflammatory phenotype and physiological decline. Specialized proresolving lipid mediators (SPMs) are endogenous autacoids that actively promote resolution of inflammation. In this study, we investigated resolution of acute inflammation in aging and the roles of SPMs. Using a self-resolving peritonitis and resolution indices coupled with lipid mediator metabololipidomics, we found that aged mice had both delayed resolution and reduced SPMs.
The SPM precursor docosahexaenoic acid accelerated resolution via increased SPMs and promoted human monocyte reprogramming. In aged mice, novel nanoproresolving medicines carrying aspirin-triggered resolvins D1 and D3 reduced inflammation by promoting efferocytosis. These findings provide evidence for age-dependent resolution pathways in acute inflammation and novel means to activate resolution.