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. 2011 Jul;24(3):557–591. doi: 10.1128/CMR.00008-11

Fig. 1.

Fig. 1.

(A) Mucus breakdown. S. pneumoniae colonization of the nasopharynx is facilitated by mucus degradation by the enzymes NanA, BgaA, StrH, and NanB. Ply decreases epithelial cell ciliary beating, enhancing bacterial adherence. (B) Evasion of proteolytic enzymes. Pneumococcal cell wall peptidoglycans may be destroyed by lysozyme. PdgA and Adr deacetylate pneumococcal cell surface petidoglycan molecules, rendering them resistant to lysozyme. (C) Epithelial cell binding. S. pneumoniae binds host GalNac by using SpxB, Smi, MsrA, and PlpA. (D) Intracellular translocation. By binding the pIgR with PspC (or PAF receptor [PAFr] with ChoP), pneumococci can use the pIgR or PAF receptor recycling pathway to be transported through the epithelial cell layer. (E) Inter- and pericellular translocation. Plasminogen bound by Gly3Ph, CbpE, and enolase enhances epithelial cell binding and degrades interepithelial adherens junctions, allowing pericellular migration.