Aging and Coronavirus: Exploring Complementary Therapies to Avoid Inflammatory Overload

摘要

Acute respiratory distress syndrome (ARDS) is the main cause of death in COVID-19 patients (1, 2). In recent years the relationship between this respiratory syndrome and inflammatory system dysregulation has been discussed (3). Patients with ARDS could present distinct endophenotypes with respect to immune alterations: hyper- or hypo-inflammatory profiles (4, 5). The identification of inflammatory endophenotypes of ARDS is important, as patients respond differently to clinical and hospital management (3). In patients with a hyper-inflammatory profile, a pro-inflammatory storm is observed in the human body, with elevated rates of biomarkers such as C Reactive Protein (CRP) (2, 6) and cytokines such as interleukins (IL)-6 and tumoral necrosis factor (TNF)-α that are able to develop a systemic inflammatory response. The release of IL-6 and TNF-α into the systemic circulation directly contributes to the increase in systemic inflammation levels and arteriosclerosis processes (7).