Inflamm-aging, that is the age-associated inflammatory status, is considered one of the most striking consequences of immunosenescence,
as it is believed to be linked to the majority of age-associated diseases sharing an inflammatory basis. Nevertheless, evidence
is emerging that inflamm-aging is at least in part independent from immunological stimuli. Moreover, centenarians who avoided or
delayed major inflammatory diseases display markers of inflammation. In this paper we proposed a reappraisal of the concept of inflamm-
aging, suggesting that its pathological effects can be independent from the total amount of pro-inflammatory mediators, but they
would be rather associated with the anatomical district and type of cells where they are produced and where they primarily act.
Keywords: Inflammation, aging, centenarians, cell senescence, immunosenescence, immunological stimuli, pro-inflammatory mediators, markers, inflamm-aging, longevity
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