Review Article

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

Figure 1

Expression and recruitment of pneumococcal binding proteins (PBPs) on different anatomical sites of the host in the order of pneumococcal binding. Host pneumococcal binding proteins pIgR and PAFr are expressed ubiquitously on epithelial and endothelial cells such as nasopharyngeal mucosal epithelial cells. Pneumococcal adhesin PsrP interacts with K10, besides CbpA and ChoP-mediated binding to pIgR, PAFr, and LR and causes pneumonia. Invasion is facilitated by PAFr, and dissemination occurs resulting in septicemia. Finally, the pneumococcus crosses the blood brain barrier by binging to the PBP, LR on the meningococcal cells, leading to pneumococcal meningitis. Red arrows indicate the sequential binding and invasion of the pneumococcus from the site of colonization to meningococcal invasion. Note the increased expression of PBPs on the lung-cell surface during aging (bottom panel) as compared to the young age.
267101.fig.001