Among its many roles, this epithelial barrier is one of the most fundamental components of the innate immune system, protecting organisms from the vast environmental microbiota indeed, >90% of infectious agents enter through mucosal epithelia. The BL surface is adapted for interaction with other cells and for exchange with the bloodstream. The AP surface serves as a barrier to the outside world and is specialized for the exchange of materials with the lumen. Many internal organs are lined by a monolayer of polarized epithelia with separate apical (AP) and basolateral (BL) surfaces that are defined by distinct protein and lipid compositions and are separated by tight junctions ( Gibson and Perrimon, 2003). The end result is that this bacterium transforms AP into BL membrane, creating a local microenvironment that facilitates its colonization and entry into the mucosal barrier. These protrusions lack AP membrane markers and are comprised of BL membrane constituents, which are trafficked there by transcytosis. Membrane protrusions enriched for PIP3 and actin accumulate at the AP surface at the site of bacterial binding. aeruginosa binds near cell–cell junctions without compromising them where it activates and recruits PI3K to the AP surface. aeruginosa subverts this pathway to gain entry from the AP surface. aeruginosa entry from the apical (AP) surface and that AP addition of phosphatidylinositol 3,4,5-trisphosphate (PIP3) is sufficient to convert AP into BL membrane (Kierbel, A., A. We previously demonstrated that activation of phosphatidylinositol 3-kinase (PI3K) and Akt are necessary and sufficient for P. Pseudomonas aeruginosa, an important human pathogen, preferentially binds and enters injured cells from the basolateral (BL) surface.

Pip3 pathway