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.
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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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    • "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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