Intestinal microbiota containing Barnesiella cures vancomycin-resistant Enterococcus faecium colonization.
ABSTRACT Bacteria causing infections in hospitalized patients are increasingly antibiotic-resistant. Classical infection control practices are only partially effective at preventing spread of antibiotic-resistant bacteria within hospitals. Because the density of intestinal colonization by the highly antibiotic-resistant bacterium vancomycin-resistant Enterococcus (VRE) can exceed 10(9) organisms per gram of feces, even optimally implemented hygiene protocols often fail. Decreasing the density of intestinal colonization, therefore, represents an important approach to limit VRE transmission. We demonstrate that reintroduction of a diverse intestinal microbiota to densely VRE colonized mice eliminates VRE from the intestinal tract. While oxygen-tolerant members of the microbiota are ineffective at eliminating VRE, administration of obligate anaerobic commensal bacteria to mice results in a billion-fold reduction in the density of intestinal VRE colonization. 16S rRNA gene sequence analysis of intestinal bacterial populations isolated from mice that cleared VRE following microbiota reconstitution revealed that re-colonization with a microbiota that contains Barnesiella correlates with VRE elimination. Characterization of the fecal microbiota of patients undergoing allogeneic hematopoietic stem cell transplantation demonstrated that intestinal colonization with Barnesiella confers resistance to intestinal domination and bloodstream infection with VRE. Our studies indicate that obligate anaerobic bacteria belonging to the Barnesiella genus enable clearance of intestinal VRE colonization and may provide novel approaches to prevent the spread of highly antibiotic-resistant bacteria.
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ABSTRACT: The human gut commensal microbiota forms a complex population of microorganisms that survive by having maintaining a symbiotic relationship with the host. Amongst the metabolic benefits it brings, formation of adaptive immune system and maintenance of its homeostasis are functions that play as important role. This review discusses the integral elements of commensal microbiota that stimulate responses of different parts of the immune system and leads to health or disease. It aims to establish conditions and factors that contribute to gut commensal microbiota's transformation from symbiotic to antibiotic relationship with human. We suggest that a the host-microbiota relationship has been evolved to benefit both parties and any changes that may lead to disease, are not due to unfriendly properties of the gut microbiota but due to host genetics or environmental changes such as diet or infection.Medicina (Kaunas, Lithuania) 03/2015; 464(2). DOI:10.1016/j.medici.2015.03.001 · 0.51 Impact Factor
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ABSTRACT: The microbiota of the human gut is gaining broad attention owing to its association with a wide range of diseases, ranging from metabolic disorders (e.g. obesity and type 2 diabetes) to autoimmune diseases (such as inflammatory bowel disease and type 1 diabetes), cancer and even neurodevelopmental disorders (e.g. autism). Having been increasingly used in biomedical research, mice have become the model of choice for most studies in this emerging field. Mouse models allow perturbations in gut microbiota to be studied in a controlled experimental setup, and thus help in assessing causality of the complex host-microbiota interactions and in developing mechanistic hypotheses. However, pitfalls should be considered when translating gut microbiome research results from mouse models to humans. In this Special Article, we discuss the intrinsic similarities and differences that exist between the two systems, and compare the human and murine core gut microbiota based on a meta-analysis of currently available datasets. Finally, we discuss the external factors that influence the capability of mouse models to recapitulate the gut microbiota shifts associated with human diseases, and investigate which alternative model systems exist for gut microbiota research. © 2015. Published by The Company of Biologists Ltd.Disease Models and Mechanisms 01/2015; 8(1):1-16. DOI:10.1242/dmm.017400 · 5.54 Impact Factor
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ABSTRACT: The three main processes shaping the evolutionary ecology of antibiotic resistance (AbR) involve the emergence, invasion and occupation by antibiotic-resistant genes of significant environments for human health. The process of emergence in complex bacterial populations is a high-frequency, continuous swarming of ephemeral combinatory genetic and epigenetic explorations inside cells and among cells, populations and communities, expanding in different environments (migration), creating the stochastic variation required for evolutionary progress. Invasion refers to the process by which AbR significantly increases in frequency in a given (invaded) environment, led by external invaders local multiplication and spread, or by endogenous conversion. Conversion occurs because of the spread of AbR genes from an exogenous resistant clone into an established (endogenous) bacterial clone(s) colonizing the environment; and/or because of dissemination of particular resistant genetic variants that emerged within an endogenous clonal population. Occupation of a given environment by a resistant variant means a permanent establishment of this organism in this environment, even in the absence of antibiotic selection. Specific interventions on emergence influence invasion, those acting on invasion also influence occupation and interventions on occupation determine emergence. Such interventions should be simultaneously applied, as they are not simple solutions to the complex problem of AbR.Evolutionary Applications 12/2014; 8(3). DOI:10.1111/eva.12235 · 4.57 Impact Factor