![]() Mechanistically, both inflammaging and immunosenescence can be promoted not only by the individual repeated exposures to different pathogens during life but also by the age-related increased burden of senescent cells ( Humphreys et al., 2020). ![]() Immune cells can themselves become senescent and acquire the SASP so that we previously coined the term ‘macroph-aging’ to describe the contribution of the senescent macrophages to inflammaging ( Prattichizzo et al., 2016). Human aging is accompanied by a complex remodeling of the immune system characterized on one hand by an increased innate immune activity ( Cunha et al., 2020), and on the other hand by a gradual decline in adaptive functions ( Lee et al., 2016, Salminen et al., 2018a). Notably, a complex cross-link exists between inflammaging and cellular senescence, since a chronic proinflammatory status can contribute to increase the amount of senescent cells and amplify a vicious circle that increases the risk to develop the most common age-related diseases ( Fulop et al., 2017, Lagnado et al., 2021). Current thinking is that the short-term presence of senescent cells in a younger milieu can promote the plasticity of neighboring cells, whereas their progressive accumulation during aging can contribute to fuel inflammaging and to spread senescence at paracrine and systemic levels ( Hernandez-Segura et al., 2018, Prata et al., 2018). During human aging, the accumulation of macromolecular damage leads to the stochastic build-up of senescent cells that fail to accomplish their normal tasks and acquire a senescence-associated pro-inflammatory phenotype (SASP) ( Coppe et al., 2008). The aging process is associated with a chronic, systemic, and low-grade proinflammatory condition previously termed as “inflammaging” ( Franceschi et al., 2000). Here, we reviewed this evidence and highlighted several circulating biomarkers of inflammaging that could provide additional prognostic information to stratify COVID-19 patients based on the risk of severe outcomes. Increasing evidence suggests that senescent myeloid and endothelial cells are characterized by the acquisition of a senescence-associated pro-inflammatory phenotype (SASP), which is considered as the main culprit of both immunosenescence and inflammaging. These age-related features of the immune system were highlighted in patients affected by COVID-19 with the poorest clinical outcomes, suggesting that the mechanisms underpinning immunosenescence and inflammaging could be relevant for COVID-19 pathogenesis and progression. Chronically and systemically activated innate immune responses and impaired antiviral responses have been recognized as the results of a progressive remodeling of the immune system during aging, which can be described by the words ‘immunosenescence’ and ‘inflammaging’. Timely diagnosis and risk stratification are crucial steps to define appropriate therapies and reduce mortality, especially in the older patients. ![]() In the older patients, COVID-19 manifests predominantly as a systemic disease associated with immunological, inflammatory, and procoagulant responses. The case fatality rate for COVID-19 grows exponentially with age and the presence of comorbidities. ![]() The COVID-19 pandemic caused by SARS-CoV-2 infection has been of unprecedented clinical and socio-economic worldwide relevance. ![]()
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