Salmonella-microbiome interactions in the gut and their impact on transmission

Microbiology Seminar Series

  • Datum: 18.11.2019
  • Uhrzeit: 13:15
  • Vortragende(r): Prof. Dr. Denise Monack
  • Stanford University, James H. Clark Center, USA
  • Ort: MPI for Terrestrial Microbiology
  • Raum: Lecture hall
  • Gastgeber: Prof. Dr. Rolf Thauer
  • Kontakt:

Disease transmission is a multifaceted process mediated by the interactions between the pathogen and host. Salmonella enterica serovars are important human enteric pathogens that cause disease ranging from self-limiting gastroenteritis to persistent systemic infections, such as typhoid fever. Transmission occurs via the fecal-oral route, and epidemiological analyses have revealed heterogeneity in host transmission capabilities. The underlying mechanisms that lead to this heterogeneity is an area of intense study. We will explore the dynamic interactions between Salmonella and the high-density polymicrobial community, the microbiota, in the distal gut. For example, the ability of Salmonella to colonize and grow in the lumen of the gut requires a type 6 secretion system (T6SS) which is encoded on a pathogenicity island. Salmonella utilizes the T6SS to inject a lethal toxin into a commensal bacterium, Klebsiella oxytoca, thus, eliminating a potential competitor. In addition to Salmonella-mediated colonization mechanisms, we will explore mechanisms by which the intestinal microbiota provides protection against this invading pathogen by limiting pathogen expansion and transmission into the environment. Previously described mechanisms of microbiota-mediated colonization resistance have been identified by observing loss of colonization resistance after community perturbations such as antibiotic treatment or diet changes. I will describe a new microbiota-mediated mechanism of colonization resistance against S. Typhimurium. By comparing high-complexity communities with different levels of colonization resistance, we demonstrate that Bacteroides species mediate colonization resistance against S. Typhimurium in vivo through the production of the short-chain fatty acid propionate. We show that propionate directly inhibits S. Typhimurium growth in vitro by disrupting intracellular pH homeostasis. We provide the first mechanistic understanding of the role of individualized microbial communities in host-to-host variability of pathogen transmission.

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