Cho I, Blaser MJ.. The human microbiome: at the interface of health and disease. Nat Rev Genet 13: 260-270

Department of Medicine, NYU Langone Medical Center, New York, New York 10016, USA.
Nature Reviews Genetics (Impact Factor: 36.98). 03/2012; 13(4):260-70. DOI: 10.1038/nrg3182
Source: PubMed


Interest in the role of the microbiome in human health has burgeoned over the past decade with the advent of new technologies for interrogating complex microbial communities. The large-scale dynamics of the microbiome can be described by many of the tools and observations used in the study of population ecology. Deciphering the metagenome and its aggregate genetic information can also be used to understand the functional properties of the microbial community. Both the microbiome and metagenome probably have important functions in health and disease; their exploration is a frontier in human genetics.

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    • "In contrast to natural strains of yeast, laboratory strains are incapable of dimorphic transition and microcolony unification into a biofilm in response to the release of volatile ammonia during the first alkali phase within microcolonies (St'ovíček et al., 2010; Vopálenská et al., 2010; Váchová and Palková, 2011). When cell growth within a colony decelerates, the colony begins to acidify medium and enters the first acidic phase (Figure 2(B)) (Palková et al., 2002; Váchová et al., 2012). "
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    ABSTRACT: Cell-autonomous mechanisms underlying cellular and organismal aging in evolutionarily distant eukaryotes have been established; these mechanisms regulate longevity-defining processes within a single eukaryotic cell. Recent findings have provided valuable insight into cell-non-autonomous mechanisms modulating cellular and organismal aging in eukaryotes across phyla; these mechanisms involve a transmission of various longevity factors between different cells, tissues and organisms. Herein, we review such cell-non-autonomous mechanisms of aging in eukaryotes. We discuss the following: (1) how low molecular weight transmissible longevity factors modulate aging and define longevity of cells in yeast populations cultured in liquid media or on solid surfaces, (2) how communications between proteostasis stress networks operating in neurons and non-neuronal somatic tissues define longevity of the nematode Caenorhabditis elegans by modulating the rates of aging in different tissues, and (3) how different bacterial species colonizing the gut lumen of C. elegans define nematode longevity by modulating the rate of organismal aging.
    International review of cell and molecular biology 10/2015; 321:in press. DOI:10.1016/bs.ircmb.2015.09.003 · 3.42 Impact Factor
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    • "Genetic variation alone cannot account for a dramatic increase in disease prevalence over such a short time frame. Emerging evidence suggests that twenty-first century environmental interventions, including widespread antibiotic use, consumption of a high-fat/low fiber diet, elimination of previously common enteropathogens (including Helicobacter pylori and helminthic parasites), reduced exposure to infectious disease, Caesarean birth, and formula feeding, may have perturbed the mutually beneficial interactions established over millions of years of coevolution with the bacteria that comprise our commensal microbiota (Cho and Blaser, 2012). This dysbiosis can predispose genetically susceptible individuals to allergic disease (reviewed in ref. "
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    ABSTRACT: Dietary intervention with extensively hydrolyzed casein formula supplemented with Lactobacillus rhamnosus GG (EHCF+LGG) accelerates tolerance acquisition in infants with cow's milk allergy (CMA). We examined whether this effect is attributable, at least in part, to an influence on the gut microbiota. Fecal samples from healthy controls (n=20) and from CMA infants (n=19) before and after treatment with EHCF with (n=12) and without (n=7) supplementation with LGG were compared by 16S rRNA-based operational taxonomic unit clustering and oligotyping. Differential feature selection and generalized linear model fitting revealed that the CMA infants have a diverse gut microbial community structure dominated by Lachnospiraceae (20.5±9.7%) and Ruminococcaceae (16.2±9.1%). Blautia, Roseburia and Coprococcus were significantly enriched following treatment with EHCF and LGG, but only one genus, Oscillospira, was significantly different between infants that became tolerant and those that remained allergic. However, most tolerant infants showed a significant increase in fecal butyrate levels, and those taxa that were significantly enriched in these samples, Blautia and Roseburia, exhibited specific strain-level demarcations between tolerant and allergic infants. Our data suggest that EHCF+LGG promotes tolerance in infants with CMA, in part, by influencing the strain-level bacterial community structure of the infant gut.
    The ISME Journal 09/2015; DOI:10.1038/ismej.2015.151 · 9.30 Impact Factor
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    • "Novel potential pathogens might include opportunistic microbes that are typical members of a human host microbiome. Only under unusual circumstances might they become pathogenic; for example when the human host becomes immune-compromised, the microbiome is altered in a manner that allows a particular microbe to reach high abundances and become pathogenic [29], or virulence increases due to a genetic or physiological change. Other examples of novel potential pathogens are those newly discovered in humans, but which do not yet cause clinical illness. "
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    ABSTRACT: Microbial infections are as old as the hosts they sicken, but interest in the emergence of pathogens and the diseases they cause has been accelerating rapidly. The term 'emerging infectious disease' was coined in the mid-1900s to describe changes in disease dynamics in the modern era. Both the term and the phenomena it is meant to characterize have evolved and diversified over time, leading to inconsistencies and confusion. Here, we review the evolution of the term 'emerging infectious disease' (EID) in the literature as applied to human hosts. We examine the pathways (e.g., speciation or strain differentiation in the causative agent vs. rapid geographic expansion of an existing pathogen) by which diseases emerge. We propose a new framework for disease and pathogen emergence to improve prioritization. And we illustrate how the operational definition of an EID affects conclusions concerning the pathways by which diseases emerge and the ecological and socioeconomic drivers that elicit emergence. As EIDs appear to be increasing globally, and resources for science level off or decline , the research community is pushed to prioritize its focus on the most threatening diseases, riskiest potential pathogens, and the places they occur. The working definition of emerging infectious diseases and pathogens plays a crucial role in prioritization, but we argue that the current definitions may be impeding these efforts. We propose a new framework for classifying pathogens and diseases as " emerging " that distinguishes EIDs from emerging pathogens and novel potential pathogens. We suggest prioritization of: 1) EIDs for adaptation and mitigation, 2) emerging pathogens for preventive measures, and 3) novel potential pathogens for intensive surveillance.
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