Stefano Salvioli, Daniela Monti, Catia Lanzarini, Maria Conte, Chiara Pirazzini, Maria Giulia Bacalini, Paolo Garagnani, Cristina Giuliani, Elisa Fontanesi, Rita Ostan, Laura Bucci, Federica Sevini, Stella Lukas Yani, Annalaura Barbieri, Laura Lomartire, Vincenzo Borelli, Dario Vianello, Elena Bellavista, Morena Martucci, Elisa Cevenini, Elisa Pini, Maria Scurti, Fiammetta Biondi, Aurelia Santoro, Miriam Capri and Claudio Franceschi Pages 1675 - 1679 ( 5 )
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.
Inflammation, aging, centenarians, cell senescence, immunosenescence, immunological stimuli, pro-inflammatory mediators, markers, inflamm-aging, longevity
Dept. Experimental Pathology, University of Bologna, Via S. Giacomo 12, 40126 Bologna (I).