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. 2021 Dec 1;17(12):e1009592. doi: 10.1371/journal.ppat.1009592

Fig 9. A working model for GC infection in the human cervix.

Fig 9

(A) GC infection in the ectocervical epithelium. Low expression levels of β-catenin and ezrin in the luminal layer of cervical epithelial cells (A lack of red color at the cell periphery indicates the low expression level of ezrin) potentially inhibit GC-induced actin (green dashed lines at the cell periphery) reorganization. GC also activate β1 integrin in ectocervical epithelial cells, which suppresses epithelial exfoliation and enhances GC adherence. (B) GC infection in the endocervical epithelium. GC interactions with the apical surface of columnar cervical epithelial cells with ezrin-actin-supported dense microvilli (ezrin, red triangles; and actin, green lines) activate NMII (orange arrows) at GC adherent sites in a Ca2+-dependent manner. The activation and reorganization of NMII induce the disassembly of both ezrin-actin networks underneath GC microcolonies and perijunctional actomyosin rings, which leads to microvilli modification and apical junction disassembly, facilitating GC transmigration across the epithelium and causing epithelial shedding. (C) GC infection in ezrin-expressing (red cell border) squamous epithelial cells. GC interactions activate ezrin (red triangles) and the accumulation of ezrin-actin (green lines) networks at GC adherent sites. This ezrin-actin reorganization drives GC contacting microvilli to elongate and wrap up bacteria, facilitating GC entry into epithelial cells. Pili is essential for initiating GC-epithelial interactions and triggering the events leading to adherence, invasion, and transmigration. Opa proteins, particularly OpaCEA, promote GC colonization and invasion by enhancing GC-induced ezrin-actin accumulation and microvilli elongation in squamous epithelial cells (C) and inhibiting GC-induced ezrin-actin disassembly and microvilli modification in columnar epithelial cells (B). OpaCEA expression also reduces GC transmigration and columnar epithelial cell shedding by inhibiting GC-induced NMII activation and apical junction disassembly (B).