Modulation of Bacterial Pathogenesis by Oppressive Aging Factors: Insights into Host-Pneumococcal Interaction Strategies

Figure 2

Integral network of cellular senescence and host-pneumococcal interaction in the aged lungs. Lung-cell senescence occurs during the inevitable process of aging. Note the onset of senescence by DNA damage and stress signals is distinctly operated by the two major signaling events, the p53/p21 and the p16/pRb pathways. Both these pathways induce SASP production and enhanced PBPs expression and recruitment. Pneumococcal binding occurs at a comparatively faster pace than under normal conditions, as shown by the binding of the elongated chains of pneumococci. Involvement of K10 as a putative feedback control in mediating cell-cycle arrest is shown as demonstrated by Paramio et al. [30, 31].