Membrane vesicle trafficking

This different phenomenon has a major role in host–pathogen interactions, endotoxic shock in patients, invasion and infection of animals or plants, inter-species bacterial competition, quorum sensing, exocytosis, and other areas.

Once vesicles are produced in the endoplasmic reticulum and modified in the Golgi body they make their way to a variety of destinations within the cell.

Once the vesicle arrives at its destination it joins with the bi-lipid layer in a process called fusion, and then releases its contents.

Receptors embedded in the membrane of the Golgi body bind specific cargo (such as dopamine) on the lumenal side of the vesicle.

[4] All these types (1–4) of modes of membrane vesicle trafficking, taking place in eukaryotic cells have been explained diagrammatically.

Bacterial outer membrane vesicles dispersion along the cell surface was measured in live Escherichia coli, commensal bacteria common in the human gut.

A role for membrane vesicles in pathogenic processes has been suspected since the 1970s, when they were observed in gingival plaque by electron microscopy.

[13] These studies brought the focus on OMVs into membrane vesicle trafficking and showed this phenomenon as involved in multifarious processes including genetic transformation, quorum sensing, competition arsenal among microbes, and invasion, infection, immuno-modulation, of animal hosts.

Here a vesicle forms as cargo, receptors and coat proteins gather. The vesicle then buds outwards and breaks free into the cytoplasm. The vesicle is moved towards its target location then docks and fuses.
Fig. 2 Membrane vesicle trafficking Mechanism (A–E), proposed for release (stages A–C) of outer membrane vesicles, OMVs from gram-negative bacteria in analogy of soap-bubble formation from a bubble-tube assembly (RC in stage C) of rivet complexes, RC, and their translocation (stage D) to animal host/target cell, TC. General secretory pathway (GSP) secretes proteins across bacterial cell membrane (CM) to bulge out lipopolysaccharide (LPS)-rich outer membrane (OM) above peptidoglycan (PDG) layer into pockets of inflated periplasm, called periplasmic organelles (PO) to pinch off OMVs containing outer membrane proteins (OMPs), secretory proteins (SP) and chaperons (CH). OMVs signal epithelial host cells (EHC) to ruffle (R) aiding macropinoctosis of gram negative (G−) microbe (stage E).
Fig. 3 Transmission electron micrograph of human Salmonella organism bearing periplasmic organelles, (p, line arrow) on its surface and releasing bacterial outer membrane vesicles (MV) being endocytosed (curved arrow) by macrophage cell (M) in chicken ileum in vivo