Colonisation resistance

Colonization resistance is the mechanism whereby the intestinal microflora protects itself against incursion by new and often harmful microorganisms.[1] Colonization resistance was first identified in 1967 and was initially referred to as antibiotic associated susceptibility. It was observed that animals being treated with the antibiotic streptomycin were susceptible to Salmonella enterica at doses 10,000 fold lower than the standard minimal infectious dose.[2] This led to investigations about the mechanisms utilized by endogenous microbial populations that conferred protection against exogenous pathogens attempting to colonize the gut flora. Recently, it has been observed that colonization resistance can occur within the host in a 'direct' or 'indirect' manner.[3] The former refers to particular components of the microbiota directly competing with exogenous pathogens for nutritional niches (e.g. Bacteroides thetaiotaomicron directly competes with Citrobacter rodentium for carbohydrates in the intestinal lumen[4]) or by producing growth inhibitors (e.g. Bacteroides thuringiensis can secrete bacteriocin that directly targets spore-forming Clostridium difficile, thus inhibiting its growth through an unknown mechanism),[5] that directly inhibit the colonizing pathogen. Indirect colonization resistance is thought to be mediated through the induction of immune responses in the host that concomitantly inhibit the colonizing pathogen. An example of this has been observed with B. thetaiotaomicron, which can induce the host to produce antimicrobial C-type lectins REGIIIγ and REGIIIβ, both anti-microbial peptides that target gram-positive bacteria.[6]

References

  1. ↑ Wilson, Michael (2005). Microbial inhabitants of humans: their ecology and role in health and disease. Cambridge University Press. ISBN 9780521841580.
  2. ↑ Bohnhoff M, Miller CP (1962). "Enhanced Susceptibility to Salmonella Infection in Streptomycin-Treated Mice". Journal of Infectious Diseases 111 (2): 117–127.(subscription required)
  3. ↑ Buffie CG, Pamer EG (2013). "Microbiota-mediated colonization resistance against intestinal pathogens" (PDF). Nature Reviews Immunology 13: 790–801. doi:10.1038/nri3535.
  4. ↑ "Regulated virulence controls the ability of a pathogen to compete with the gut microbiota". Science 336 (6086): 1325–1329. 2012. doi:10.1126/science.1222195.
  5. ↑ Rea, MC, Sit CS, Clayton E, O'Connor PM, Whittal RM, Zheng J, Vederas JC, Ross RP, Hill C. "Thuricin CD, a posttranslationally modified bacteriocin with a narrow spectrum of activity against Clostridium difficile". Proceedings of the National Academy of Sciences of the United States of America 107 (20): 9352–9357. doi:10.1073/pnas.0913554107.
  6. ↑ Cash HL, Whitham CV, Behrendt CL, Hooper LV (25 August 2006). "Symbiotic bacteria direct expression of an intestinal bactericidal lectin". Science 313 (5790): 1126–1130. doi:10.1126/science.1127119.
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