In 2000, Franceschi et al. [1] coined the term “inflammaging” in order to refer to a low-grade pro-inflammatory status appearing during the aging process. They emphasized the role of macrophages as well as cellular stress and genetic factors in the generation of the inflammaging condition. In addition, they hypothesized that this inflammatory environment could predispose the organism to the development of several age-related diseases. During recent years, this scenario has been confirmed by a plethora of experimental evidence. However, it seems that concurrently with the chronic, low-level inflammation one encounters several symptoms of immunosenescence, both in the innate and adaptive immune systems [2,3]. The presence of a pro-inflammatory phenotype in aged mammals is evident by (i) increased expression of genes linked to inflammation and immune responses in the tissues of old humans and rodents [4-6], (ii) higher level of cytokines in serum, e.g. IL-6 and TNF-α [7,8], (iii) activation of NF-κB signaling which is the master regulator of inflammatory responses [9-11]. There are tissue specific differences in the production of age-related inflammatory factors as well as in the onset and level of pathological changes [12].
