Host-pathogen interface

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In cellular biology, the host-pathogen interface refers to the exchange of biochemical signals that occurs when a microbe encounters its host or target cell. Such cross-talk between the two can result in either a symbiotic or hostile cross-fire. In certain locations, such as the gastro-intestinal tract, the animal host's intestinal mucous-lining on the host-cell external surface may prevent a food-poisoning pathogen from achieving physical adhesion to the plasma membrane of the host cell. In addition, the arsenal of anti-microbial peptides and defensins secreted by the host can damage the integrity of the approaching microbial pathogens. Innate and cellular immunity of the animal host may also neutralize the pathogens before they come in close contact with specific host or target cells. Gram-negative bacterial pathogens having an additional outer membrane consisting largely of endotoxic lipopolysaccharide (LPS), membrane-pore forming porins, and some other outer membrane proteins, providing an apparent advantage compared to Gram-positive microbes, which lack outer membrane. Thus Gram-negative organisms have an additional storage compartment called a periplasm, a cellular space between bacterial outer membrane and the inner membrane. The periplasm allows special attributes to the Gram negative organisms, as this compartment can expand to accommodate increasing amounts of microbial secretions; it can also 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[edit]

Role in mimicry of host enzymes[edit]

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[edit]

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 actin cytoskeleton by Salmonella pathogens for entering into host cells.[6] The host-pathogen interface is also an important subject of study, especially when pathogens come in close encounter with host body defence cells like macrophages and hijack these defence cells for their purposes, such as spreading the malaise into a systemic mode of infection by pathogens. This is noticed from observably high multiplication of Salmonella pathogens in cytoplasm of movement-prone macrophages, which are proposed to be signaled into apoptosis. Apoptosis of macrophages has been suggested to be induced by pathogen biochemical signals translocated to macrophages via OMVs secreted by host-interactive salmonellae at the host-pathogen interface.[7] Salmonella-induced macrophage death may occur via multiple mechanisms with different outcomes.[8] The host-pathogen interface may also involve a physical contact between the eukaryotic host cells and prokaryotic microbes, so as to induce physiological and morphological changes to produce surface appendages on host-interactive salmonellae, in vitro cell cultures and named invasosomes,[9] and described as periplasmic protrusions, while studying Salmonella injected in chicken ileum in vivo.[10][11] A structural model was proposed for these bacterial surface features later and these appendages were re-designated with more general name, periplasmic organelles.[12]

Role in host atopy and allergy[edit]

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[edit]

References[edit]

  1. ^ YashRoy, R.C. (1998). "Discovery of vesicular exocytosis in prokaryotes and its role in Salmonella invasion". Current Science 75 (10): 1062–1066. 
  2. ^ Beveridge, T.J. (1999). "Structures of gram-negative cell walls and their derived membrane vesicles". Journal of Bacteriology 181 (16): 4725–4733. PMC 93954. PMID 10438737. 
  3. ^ Hicks, S.W.; Galan, J.E. (2013). "Exploitation of eukaryotic subcellular targeting mechanisms by bacterial effectors". Nature Reviews Microbiology 11 (5): 316–326. doi:10.1038/nrmicro3009. PMC 3859125. PMID 23588250. 
  4. ^ Hicks, S.W.; Galan, J.E. (2010). "Hijacking the host ubiquitin pathway: structural strategies of bacterial E3 ubiquitin ligases". Current Opinion in Microbiology 13 (1): 41–46. doi:10.1016/j.mib.2009.11.008. PMC 2822022. PMID 20036613. 
  5. ^ Patel, J.C.; Rossanese, O.W.; Galan, J.E. (2005). "The functional interface between Salmonella and its host cell: opportunities for therapeutic intervention". Trends in Pharmacological Science 26 (11): 564–570. doi:10.1016/j.tips.2005.09.005. PMID 16182381. 
  6. ^ Patel, J.C.; Galan, J.E. (2005). "Manipulation of the host actin cytoskeleton by Salmonella -- all in the name of entry.". Current Opinion in Microbiology 8 (1): 10–15. doi:10.1016/j.mib.2004.09.001. PMID 15694851. 
  7. ^ YashRoy, R.C. (2000). "Hijacking of macrophages by Salmonella (3,10:r:-) through 'Type III' secretion-like exocytotic signaling: A mechanism for infection in chicken ileum". Indian Journal of Poultry Science 35 (3): 276–281. 
  8. ^ Hueffer, K.; Galan, J.E. (2004). "Salmonella-induced macrophage cell death: multiple mechanisms, different outcomes". Cellular Microbiology 6 (11): 1019–1025. doi:10.1111/j.1462-5822.2004.00451.x. PMID 15469431. 
  9. ^ Ginocchio, C.; Olmsted, S.; Wells, C.; Galan, J.E. (1994). "Contact with epithelial cells induces the formation of surface appendages on Salmonella typhimurium". Cell 76: 717–724. doi:10.1016/0092-8674(94)90510-x. 
  10. ^ YashRoy, R.C. (1992). "Salmonella 3,10:r:- surface interactions with intestinal epithelial cell microvilli". Indian Journal of Animal Sciences 62 (6): 502–504. 
  11. ^ YashRoy, R.C. (1993). "Electron microscope studies on surface pili and vesicles of Salmonella 3,10:r:- organisms". Indian Journal of Animal Sciences 63 (2): 99–102. 
  12. ^ YashRoy, R.C. (2003). "Eucaryotic cell intoxication by Gram-negative pathogens: A novel bacterial outermembrane-bound vesicular exocytosis model for Type III secretion system". Toxicology International 10 (1): 1–9. 
  13. ^ Brown, E.M.; Arrieta, M.C.; Finlay, B.B. (2013). "A fresh look at the hygiene hypothesis: how intestinal microbial exposure drives immune effector responses in atopic diseases". Semin Immunology 25 (5): 378–87. doi:10.1016/j.smim.2013.09.003. PMID 24209708. 
  14. ^ Russel, S.L.; Finlay, B.B. (2012). "The impact of gut microbes in allergic diseases". Current Opinion in Gastroenterology 28 (6): 563–569. doi:10.1097/MOG.0b013e3283573017. PMID 23010680. 
  15. ^ Brown, E. M.; Sadarangani, M; Finlay, B. B. (2013). "The role of the immune system in governing host-microbe interactions in the intestine". Nature Immunology 14 (7): 660–7. doi:10.1038/ni.2611. PMID 23778793.