Antimicrobial peptide resistance mediates resilience of prominent gut commensals during inflammation

Science  09 Jan 2015:
Vol. 347, Issue 6218, pp. 170-175
DOI: 10.1126/science.1260580

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Gut microbes resist inflammation

It is vital to human well-being that our gut microbiota can be distinguished from harmful, but often very similar, organisms. Cullen et al. begin to analyze how one dominant symbiont, Bacteroidetes thetaiotaomicron, does this. Our guts release potent antimicrobial peptides when we become infected with pathogenic bacteria such as salmonella, but these symbionts make an outer lipopolysaccharide coat that differs from those of pathogens by only one phosphate molecule. Enzymatic removal of this group is enough to confer resistance to the host's immune response and allow the symbionts to escape damage.

Science, this issue p. 170


Resilience to host inflammation and other perturbations is a fundamental property of gut microbial communities, yet the underlying mechanisms are not well understood. We have found that human gut microbes from all dominant phyla are resistant to high levels of inflammation-associated antimicrobial peptides (AMPs) and have identified a mechanism for lipopolysaccharide (LPS) modification in the phylum Bacteroidetes that increases AMP resistance by four orders of magnitude. Bacteroides thetaiotaomicron mutants that fail to remove a single phosphate group from their LPS were displaced from the microbiota during inflammation triggered by pathogen infection. These findings establish a mechanism that determines the stability of prominent members of a healthy microbiota during perturbation.

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