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Host-pathogen interface

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Title: Host-pathogen interface  
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Subject: Cellular communication (biology), Bacterial outer membrane, Membrane vesicle trafficking, Vesicle (biology and chemistry), Infection
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Host-pathogen interface

In bleb out nanovesicles, called bacterial outer membrane vesicles, (OMVs). These OMVs can translocate a variety of biochemical signal molecules to other target cells of its own type (intra-species) for quorum sensing or other competing microbes (inter-species) to thwart them from sharing the same nutritional niche, or to animal/plant eukaryotic cells for inter-kingdom interactions. OMVs thus open a new vista in the important field of membrane vesicle trafficking. This was heralded as a revolutionary process of vesicular exocytosis in prokaryotes for multiple purposes, including invasion of animal hosts,[1] and inter-bacterial interactions.[2]

Animal host - Bacterial pathogen interface examples

Role in mimicry of host enzymes

Bacterial signals/effectors exploit host cell machinery to accurately target host's biochemical activities in favour of the microbe.[3]

Bacterial effectors, upon entry into host cell cytosol, can also mimic the activity of eukaryotic enzymes, E3 ubiquitin ligases, which in turn, may interfere with eukaryotic host cell regulation of vesicular trafficking, cell cycle progression and inflammatory response.[4] It is expected that analysis of the atomic interface at the host-pathogen cross-talk platform may provide the possibility of designing novel therapeutics to disrupt disease and infection processes at molecular levels.[5]

Role in host invasion

Fig 1 Panoramic view of ultrastructure of host-pathogen interface in vivo. Human pathogens Salmonella 3,10:r:- interacting with chicken ileum. Host-interactive pathogens (Sal) develop numerous 'invasosomal' surface blebs called periplasmic organelles (PO), which seemingly pinch off as bacterial outer membrane vesicles (OMV), implicated in translocation of bacterial signals to host epithelial cells for focal disruption of microvilli, ruffle formation and creation of a safe passage (corridor) for invasion of salmonellae. OMV release is proposed to be aided by type III secretion injectisome-like rivet complexes arranged into a 'bubble tube like' assembly, operating in analogy to soap bubble release.

Host-pathogen interface signaling mechanisms have unique multifunctional role in temporal regulation of key effectors in manipulation of host [12]

Role in host atopy and allergy

Host-pathogen interface at the level of intestinal microbiota-immune system interplay has also been suggested to be responsible for atopic[13] and allergic diseases too.[14] Although microbiota is responsible for development of host immune system, yet host immune responses also regulate the structure and composition of the host intestinal microbiota.[15]

See also

References

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