Colonization resistance is the mechanism whereby themicrobiome protects itself against incursion by new and often harmfulmicroorganisms.[1][2][3]
Colonization resistance was first identified in 1967, and it was initially referred to asantibiotic-associated susceptibility. It was observed that animals being treated with the antibioticstreptomycin were susceptible toSalmonella enterica at doses 10,000 fold lower than the standard minimal infectious dose.[4] This led to investigations about the mechanisms utilized by endogenous microbial populations that conferred protection against exogenous pathogens attempting tocolonize thegut flora.
It has been observed that colonization resistance can occur within the host in a 'direct' or 'indirect' manner.[5] The former refers to particular components of the microbiota directly competing with exogenous pathogens for nutritional niches (e.g.E. coli directly competes withCitrobacter rodentium forcarbohydrates in theintestinal lumen[6]) or by producing growth inhibitors (e.g.Bacteroides thuringiensis can secretebacteriocin that directly targets spore-formingClostridioides difficile, thus inhibiting its growth through an unknown mechanism),[7] that directly inhibit the colonizing pathogen. Indirect colonization resistance is thought to be mediated through the induction ofimmune responses in the host that concomitantly inhibit the colonizing pathogen. An example of this has been observed withB. thetaiotaomicron, which can induce the host to produce antimicrobial C-type lectinsREGIIIγ andREGIIIβ, both anti-microbial peptides that targetgram-positive bacteria.[8]
Scientists found that gut infections increase its microbiota's resistance to subsequent infections, thattaurine is used in as a nutrient to nourish and train the microbiota for this by potentiating its production of sulfide and that the exogenous supply of taurine can induce this microbiota alteration.[9][10]
^Bohnhoff M, Miller CP (1962). "Enhanced Susceptibility to Salmonella Infection in Streptomycin-Treated Mice".Journal of Infectious Diseases.111 (2):117–127.doi:10.1093/infdis/111.2.117.PMID13968487.(subscription required)
