Alterung von Lunge und Immunsystem als Meilensteine in der Pathogenese von idiopathischer Lungenfibrose und COVID-19

Idiopathic pulmonary fibrosis (IPF) does not occur in younger persons. Therefore, it is not surprising that the nine hallmarks of biological aging can all be found in the pathomechanism of IPF. In this respect the homeostasis of cellular protein synthesis, degradation and recycling becomes unbalanced, which causes a dysregulation of repair mechanisms in the case of lung damage. Severve acute respiratory syndrome coronarvius type 2 (SARS-CoV-2) infections may also predominantyl seen in aged persons. In this situation cellular aging of the lungs also plays a role but additionally, the aging of the immune system is also of great importance. Immunosenescence is associated with a loss of naïve T‑cells. Moreover, there are gender-specific differences with a loss of B‑cells only in men but not in women, which partly explains the more severe course of COVID-19 pneumonia in older men.