The use of antibiotics can alter the composition of the commensal gut microbiota, which increases host susceptibility to infection by opportunistic pathogens. Now, a study shows that manipulating the levels of the quorum sensing signalling molecule autoinducer 2 (AI-2) in the mouse gut can promote growth of specific members of the microbiota that are important during recovery from antibiotic-induced dysbiosis.
The mouse gut microbiota comprises multiple bacterial species that predominately belong to the Bacteroidetes and Firmicutes phyla. Treatment with streptomycin causes a severe reduction in the overall bacterial diversity in the mouse gut; in particular, Firmicutes are almost completely depleted, whereas the relative abundance of Bacteroidetes is enriched.
As the communication between different bacterial species can influence the composition of the gut microbiota, Thompson, Oliveira et al. investigated the potential of using quorum sensing signals to modulate the bacterial composition of the mouse gut following antibiotic treatment. The authors generated an Escherichia coli strain that overproduces AI-2 — which is an interspecies quorum sensing signal — by deleting lsrK, which encodes a signal kinase that regulates AI-2 retention and degradation; the absence of LsrK led to the accumulation of extracellular AI-2. Notably, this E. coli mutant was able to stably colonize the gut of antibiotic-treated mice, which resulted in an alteration of the overall composition of bacterial species in the gut and a substantial increase in the abundance of Firmicutes, which had been severely reduced due to the antibiotic treatment.
AI-2 ... enables the initial expansion of Firmicutes in the antibiotic-treated gut microbiota
Finally, the authors compared the potential of Firmicutes and Bacteroidetes to produce AI-2 by analysing the presence of orthologues of the E. coli AI-2 synthase LuxS in sequenced bacterial genomes. Interestingly, more than 80% of the genomes from bacteria belonging to Firmicutes contained putative LuxS orthologues, whereas less than 20% of Bacteroidetes genomes encoded such genes. The increased potential of Firmicutes to synthesize AI-2 led the authors to propose a model in which AI-2 production by the mutant E. coli strain enables the initial expansion of Firmicutes in the antibiotic-treated gut microbiota; this triggers a positive feedback loop in which increased availability of AI-2 promotes the expansion of AI-2 producers.
Collectively, these data demonstrate the potential of using bacteria that produce quorum sensing signals to modulate the composition of the gut microbiota following antibiotic treatment.
Thompson, J. A., Oliveira, R. A. et al. Manipulation of the quorum sensing signal AI-2 affects the antibiotic-treated gut microbiota. Cell Rep. 10, 1861–1871 (2015)
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Nunes-Alves, C. Taking advantage of quorum sensing. Nat Rev Microbiol 13, 252 (2015). https://doi.org/10.1038/nrmicro3477
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