Do Pathogenic Chronic Infections Cause Host Senescence?

Abstract

hemoglobin molecules (hemichromes), are recognized as antigens by autologous IgG antibodies and complement system. With the deposition of a critical density of antibodies and complement molecules, senescent red blood cells are recognized and eliminated [5]. The senescent red blood cells expose phosphatidylserine on the outer portion of their plasma membrane, a sign that indicates that the cell should be phagocytosed. In healthy cells this phospholipid is actively maintained in the cytoplasmic portion of the plasma membrane. Concomitantly, there is down-regulation of the CD47 molecule, a transmembrane protein whose normal expression indicates a non-phagocytic signal. The exposure of phosphatidylserine coupled with the reduction of CD47 expression stimulates phagocytosis and the elimination of these red blood cells [6]. In 2001, Bratosin [7] and colleagues described a process similar to apoptosis occurring in red blood cells, later called erythrosis [8]. Eryptosis has several similarities to apoptosis, regardless of the trigger, induction of an eripotic state usually involves extracellular calcium entry into the cell, caspase and calpain activation, which causes changes in membrane asymmetry, phosphatidylserine exposure and cell shrinkage. and membrane.