| Autor: |
Mancuso CP; Institute for Medical Engineering and Sciences, Massachusetts Institute of Technology; Cambridge, MA 02142, USA.; Department of Civil and Environmental Engineering, Massachusetts Institute of Technology; Cambridge, MA 02142, USA., Baker JS; Institute for Medical Engineering and Sciences, Massachusetts Institute of Technology; Cambridge, MA 02142, USA.; Department of Civil and Environmental Engineering, Massachusetts Institute of Technology; Cambridge, MA 02142, USA., Qu E; Institute for Medical Engineering and Sciences, Massachusetts Institute of Technology; Cambridge, MA 02142, USA.; Department of Civil and Environmental Engineering, Massachusetts Institute of Technology; Cambridge, MA 02142, USA., Tripp AD; Institute for Medical Engineering and Sciences, Massachusetts Institute of Technology; Cambridge, MA 02142, USA.; Department of Civil and Environmental Engineering, Massachusetts Institute of Technology; Cambridge, MA 02142, USA.; Department of Systems Biology, Harvard University; Cambridge, MA 02138, USA., Balogun IO; Institute for Medical Engineering and Sciences, Massachusetts Institute of Technology; Cambridge, MA 02142, USA.; Department of Civil and Environmental Engineering, Massachusetts Institute of Technology; Cambridge, MA 02142, USA., Lieberman TD; Institute for Medical Engineering and Sciences, Massachusetts Institute of Technology; Cambridge, MA 02142, USA.; Department of Civil and Environmental Engineering, Massachusetts Institute of Technology; Cambridge, MA 02142, USA.; Broad Institute of MIT and Harvard; Cambridge, MA 02142, USA.; Ragon Institute of MGH, MIT, and Harvard; Cambridge, MA 02142, USA. |
| Abstrakt: |
Determining why only a fraction of encountered or applied bacterial strains engraft in a given person's microbiome is crucial for understanding and engineering these communities 1 . Previous work has established that metabolism can determine colonization success in vivo 2-4 , but relevance of bacterial warfare in preventing engraftment has been less explored. Here, we demonstrate that intraspecies warfare presents a significant barrier to strain transmission in the skin microbiome by profiling 14,884 pairwise interactions between Staphylococcus epidermidis cultured from eighteen human subjects from six families. We find that intraspecies antagonisms are abundant; these interactions are mechanistically diverse, independent of the relatedness between strains, and consistent with rapid evolution via horizontal gene transfer. Ability to antagonize more strains is associated with reaching a higher fraction of the on-person S. epidermidis community. Moreover, antagonisms are significantly depleted among strains residing on the same person relative to random assemblages. Two notable exceptions, in which bacteria evolved to become sensitive to antimicrobials found on the same host, are explained by mutations that provide phage resistance, contextualizing the importance of warfare among other lethal selective pressures. Taken together, our results emphasize that accounting for intraspecies bacterial warfare is essential to the design of long-lasting probiotic therapeutics. |
