PROGRAM
14:00-17:00 (WEST) // 15:00-18:00 (CEST)
Lisbon time (WEST)
14:00 Welcome by Karina Xavier
14:05 Barbel Stecher "Microbiota-dependent mechanisms of colonization resistance against intestinal pathogens."
14:45 Q&A discussion
15:00 Camille Goemans "The impact of protein synthesis inhibitors on gut microbes."
15:30 Q&A discussion
15:45 Coffee Break
16:15 Carles Ubeda "Role of the microbiome in the defense against antibiotic-resistant pathogens."
16:45 Q&A discussion
17:00 END
ABSTRACTS
Barbel Stecher
Using simplified communities to understand ecology and evolution of the gut microbiome Human gut microbial communities harbor hundreds of bacteria that form complex metabolic networks. Both pair-wise and higher-order interactions are the basis of community functionality. The lack of suitable model systems has limited our current understanding of how individual community members shape host-microbiota interactions and resistance to infections. To this end, we are using synthetic bacterial communities (Symcoms) that we can study in silico, in vitro and in gnotobiotic mouse models. Our recent data reveal how individual strains within a bacterial consortium interact, how this is influenced by the environment and how interactions translate into complex microbiome functions such as resistance to pathogen infections. Moreover, we employ model communities to study the impact of phages and antibiotics on colonization resistance and within-host evolution of the microbiome. Our long-term goal is to develop strategies to steer microbial communities towards beneficial interactions promoting human health.
Camille Goemans
The impact of protein synthesis inhibitors on gut microbes Macrolides and tetracyclines are widely-used protein synthesis inhibitors (PSIs) that have been associated with strong gut microbiota dysbiosis and long-term impact on host health and development. Their targets and modes of action have been extensively studied (primarily using model organisms and common pathogens): they have been shown to inhibit bacterial growth by blocking translation and are considered textbook bacteriostatic antibiotics. In a screen characterizing 144 antibiotics on 38 representative human gut microbiome species, we found that both macrolides and tetracyclines inhibited nearly all commensals tested but also killed several species. Killed bacteria were more readily eliminated from in vitro communities than those inhibited. In an ongoing project, we are trying to understand what underlines the killing of specific bacteria by PSIs by comparing two E. coli strains (BW25113 and ED1a) that share the same MICs for tetracycline but exhibit very different survival rates. Altogether, this species-specific killing activity challenges the long-standing distinction between bactericidal and bacteriostatic antibiotic classes and provides a possible explanation for the strong effect of macrolides on animal and human gut microbiomes.
Carles Ubeda
Role of the microbiome in the defense agains antibiotic-resistant pathogens Infections by antibiotic resistant pathogens (ARPs) including vancomycin-resistant Enterococcus (VRE) or multidrug-resistant Enterobacteriaceae (MRE) are life-threatening to patients. The intestinal microbiome protects against ARPs gut colonization, but antibiotics cause collateral damage to commensals and open the way to colonization and subsequent infection. Despite the significance of this problem, the specific commensals and mechanisms that restrict ARPs colonization remain largely unknown. Using in vitro models, mouse models of infection and multi-omic techniques to characterize the murine and human microbiome, we have identified commensal bacteria that are key for restricting VRE or MRE intestinal colonization. Moreover, we have shown that these commensal bacteria can confer protection against ARPs by producing inhibitory molecules or by competing for nutrient sources. In addition, we have demonstrated that some mechanisms of colonization resistance require cooperation between commensals. Our results could lead to novel microbiome-based therapeutic approaches in order to prevent infections by pathogens resistant to nearly all available antibiotics.