Salmonella typhimurium intercepts Escherichia coli signaling to enhance antibiotic tolerance.
Bacterial communication plays an important role in many population-based phenotypes and interspecies interactions, including those in host environments. These interspecies interactions may prove critical to some infectious diseases, and it follows that communication between pathogenic bacteria and commensal bacteria is a subject of growing interest. Recent studies have shown that Escherichia coli uses the signaling molecule indole to increase antibiotic tolerance throughout its population. Here, we show that the intestinal pathogen Salmonella typhimurium increases its antibiotic tolerance in response to indole, even though S. typhimurium does not natively produce indole. Increased antibiotic tolerance can be induced in S. typhimurium by both exogenous indole added to clonal S. typhimurium populations and indole produced by E. coli in mixed-microbial communities. Our data show that indole-induced tolerance in S. typhimurium is mediated primarily by the oxidative stress response and, to a lesser extent, by the phage shock response, which were previously shown to mediate indole-induced tolerance in E. coli. Further, we find that indole signaling by E. coli induces S. typhimurium antibiotic tolerance in a Caenorhabditis elegans model for gastrointestinal infection. These results suggest that the intestinal pathogen S. typhimurium can intercept indole signaling from the commensal bacterium E. coli to enhance its antibiotic tolerance in the host intestine.
Howard Hughes Medical Institute, Boston University, Boston, MA 02215, USA.
Nicole M
NM
Vega
Kyle R
KR
Allison
Amanda N
AN
Samuels
Mark S
MS
Klempner
James J
JJ
Collins
D000818:Animals; D000900:Anti-Bacterial Agents / Q000494:pharmacology*; D017173:Caenorhabditis elegans / Q000472:pathogenicity; D004352:Drug Resistance, Microbial; D004926:Escherichia coli / Q000187:drug effects / Q000378:metabolism*; D006373:Helminthiasis / Q000473:pathology; D012486:Salmonella typhimurium / Q000187:drug effects / Q000502:physiology*; D015398:Signal Transduction
D000900:Anti-Bacterial Agents