Gut microbiota disturbance during antibiotic therapy: A multi-omic approach

It is known that the gastrointestinal tract (GIT) microbiota responds to different antibiotics in different ways and that while some antibiotics do not induce disturbances of the community, others drastically influence the richness, diversity, and prevalence of bacterial taxa. However, the metabolic consequences thereof, independent of the degree of the community shifts, are not clearly understood. In a recent article, we used an integrative OMICS approach to provide new insights into the metabolic shifts caused by antibiotic disturbance. The study presented here further suggests that specific bacterial lineage blooms occurring at defined stages of antibiotic intervention are mostly associated with organisms that possess improved survival and colonization mechanisms, such as those of the Enterococcus, Blautia, Faecalibacterium, and Akkermansia genera. The study also provides an overview of the most variable metabolic functions affected as a consequence of a β-lactam antibiotic intervention. Thus, we observed that anabolic sugar metabolism, the production of acetyl donors and the synthesis and degradation of intestinal/colonic epithelium components were among the most variable functions during the intervention. We are aware that these results have been established with a single patient and will require further confirmation with a larger group of individuals and with other antibiotics. Future directions for exploration of the effects of antibiotic interventions are discussed.The whole consortium was funded by the Spanish Ministry of Economy and Competitiveness and the Federal Ministry of Education and Research (BMBF) within the ERA NET PathoGenoMics2 program, grant number 0315441A. This work was further funded by grants BFU2008-04501-E, SAF2009-13032-C02–01, SAF2012-31187, and CSD2007-00005 from the Spanish Ministry of Economy and Competitiveness, Prometeo/2009/092 from Generalitat Valenciana (Spain), and AGL2006-11697/ALI. The authors gratefully acknowledge the financial support provided by the European Regional Development Fund (ERDF) and the European Union (FP7 project Systems medicine of chronic inflammatory bowel disease, Grant Agreement no. 305564). This work has been partially supported by the EVASYON study funded by the Spanish Ministry of Health and Consumption (Carlos III Institute of Health. FIS Grant PI 051579).Peer Reviewe