肠道菌群紊乱和自闭症2
Semin Immunopathol. 2015 Jan;37(1):5-16. doi: 10.1007/s00281-014-0456-2. Epub 2014 Oct 22.
Toward the comprehensive understanding of the gut ecosystem via metabolomics-bad integrated omics approach.
Aw W1, Fukuda S.
Author information
∙ 1Institute for Advanced Biosciences, Keio University, 246-2 Mizukami, Kakuganji, Tsuruoka, Yamagata, 997-0052, Japan.
Abstract
Recent advances in DNA quencing and mass spectrometry technologies have allowed us
to collect more data on microbiome and metabolome to asss the influence of the gut microbiota on human health at a whole-systems level. Major advances in metagenomics and metabolomics technologies have shown that the gut microbiota contributes to host overall health status to a large extent. As such, the gut microbiota is often likened to a measurable and functional organ consisting of prokaryotic cells, which creates the unique gut ecosystem together with the host eukaryotic cells. In this review, we discuss in detail the relationship between gut microbiota and its metabolites like choline, bile acids, phenols, and short-chain fatty acids in the host health and etiopathogenesis of various pathological states such as multiple sclerosis, autism, obesity, diabetes, and chronic kidney dia. By integrating metagenomic and metabolomic information on a systems biology-wide approach, we would be better able to understand this interplay between gut microbiome and host metabolism. Integration of the microbiome, metatranscriptome, and metabolome information will pave the way toward an improved holistic understanding of the complex mammalian superorganism. Through the modeling of metabolic interactions between lifes
tyle, diet, and microbiota, integrated omics-bad understanding of the gut ecosystem is the new avenue, providing exciting novel therapeutic approaches for optimal host health.
Proc Nutr Soc. 2014 Oct 14:1-6. [Epub ahead of print]
Nutritional management of (some) autism: a ca for gluten- and cain-free diets?
Whiteley P1.
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∙ 1ESPA Rearch,2A Hylton Park,Hylton Park Road,Sunderland SR5 3HD,UK.
Abstract
Autism spectrum disorders reprent a diver and heterogeneous array of conditions unified by the variable prence of specific behaviours impacting social and communicative functions (social affect) alongside other prentation. Common overt char
acteristics may come about as a conquence of veral different genetic and biological process differentially manifesting across different people or groups. The concept of plural 'autisms' is evolving, strengthened by an increasingly important evidence ba detailing different developmental trajectories across the autismspectrum and the appearance of comorbidity variably interacting with core symptoms and onwards influencing quality of life. Reports that dietary intervention, specifically the removal of foods containing gluten and/or cain from the diet, may impact on the prentation of autism for some, complement this plural view of autism. Evidence suggestive of differing respons to the u of a gluten- and cain-free diet, defined as best- and non-respon, has combined with some progress on determining the underlying genetic and biological correlates potentially related to such dietary elements. The preliminary suggestion of a possible diet-related autism phenotype is the result. This review will highlight veral pertinent aspects onwards to an effect of food in some cas of autism including rearch on the pharmacological activity of food metabolites, immune respon, issues with gut barrier function and some contribution from the gut microbiota.
The reprent promising areas in need of far greater rearch inspection in order to potentially define such a diet-related subgroup on the autism spectrum.
Adv Exp Med Biol. 2014;817:373-403. doi: 10.1007/978-1-4939-0897-4_17.
The impact of microbiota on brain and behavior: mechanisms & therapeutic potential.
Borre YE1, Moloney RD, Clarke G, Dinan TG, Cryan JF.
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∙ 1Laboratory of NeuroGastroenterology, Alimentary Pharmabiotic Centre, University College Cork, Cork, Ireland.
Abstract
There is increasing evidence that host-microbe interactions play a key role in maintaining homeostasis. Alterations in gut microbial composition is associated with marked changes
in behaviors relevant to mood, pain and cognition, establishing the critical importance of the bi-directional pathway of communication between the microbiota and the brain in health and dia. Dysfunction of the microbiome-brain-gut axis has been implicated in stress-related disorders such as depression, anxiety and irritable bowel syndrome and neurodevelopmental disorders such as autism. Bacterial colonization of the gut is central to postnatal development and maturation of key systems that have the capacity to influence central nervous system (CNS) programming and signaling, including the immune and endocrine systems. Moreover, there is now expanding evidence for the view that entericmicrobiota plays a role in early programming and later respon to acute and chronic stress. This view is supported by studies in germ-free mice and in animals expod to pathogenic bacterial infections, probiotic agents or antibiotics. Although communication between gut microbiota and the CNS are not fully elucidated, neural, hormonal, immune and metabolic pathways have been suggested. Thus, the concept of a microbiome-brain-gut axis is emerging, suggesting microbiota-modulating strategies may be a tractable therapeutic approach for developing novel treatments for CNS disorders.
Adv Exp Med Biol. 2014;817:319-56. doi: 10.1007/978-1-4939-0897-4_15.
Microbiota, immunoregulatory old friends and psychiatric disorders.
Rook GA1, Raison CL, Lowry CA.
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∙ 1Centre for Clinical Microbiology, UCL (University College London), Royal Free Campus, Rowland Hill Street, London, NW3 2PF, UK, g.rook@ucl.ac.uk.
Abstract
Regulation of the immune system is an important function of the gut microbiota. Increasing evidence suggests that modern living conditions cau thegut microbiota to deviate from the form it took during human evolution. Contributing factors include loss of helminth infections, encountering less microbial biodiversity, and modulation of the microbiota composition by diet and antibiotic u. Thus the gut microbiota is a major
mediator of the hygiene hypothesis (or as we prefer, "Old Friends" mechanism), which describes the role of organisms with which we co-evolved, and that needed to be tolerated, as crucial inducers of immunoregulation. At least partly as a conquence of reduced exposure to immunoregulatory Old Friends, many but not all of which resided in the gut, high-income countries are undergoing large increas in a wide range of chronic inflammatory disorders including allergies, autoimmunity and inflammatory bowel dias. Depression, anxiety and reduced stress resilience are comorbid with the conditions, or can occur in individuals with persistently raid circulating levels of biomarkers of inflammation in the abnce of clinically apparent peripheral inflammatory dia. Moreover poorly regulated inflammation during pregnancy might contribute to brain developmental abnormalities that underlie some cas of autism spectrum disorders and schizophrenia. In this chapter we explain how the gut microbiota drives immunoregulation, how faulty immunoregulation and inflammation predispo to psychiatric dia, and how psychological stress drives further inflammation via pathways that involve the gut and microbiota. We also outline how this two-way relations
hip between the brain and inflammation implicates themicrobiota, Old Friends and immunoregulation in the control of stress resilience.
Trends Mol Med. 2014 Sep;20(9):509-18. doi: 10.lmed.2014.05.002. Epub 2014 Jun 20.
Microbiota and neurodevelopmental windows: implications for brain disorders.
Borre YE1, O'Keeffe GW2, Clarke G3, Stanton C4, Dinan TG3, Cryan JF5.
Author information
∙ 1Laboratory of NeuroGastroenterology, Alimentary Pharmabiotic Centre, University College Cork, Cork, Ireland.
∙ 2Department of Anatomy and Neuroscience, University College Cork, Cork, Ireland; The Irish Centre for Fetal and Neonatal Translational Rearch (INFANT), Cork University Maternity Hospital, Cork, Ireland.
∙ 3Laboratory of NeuroGastroenterology, Alimentary Pharmabiotic Centre, University College Cork, Cork, Ireland; Department of Psychiatry, University College Cork, Cork, Ireland.
∙ 4Department of Psychiatry, University College Cork, Cork, Ireland; Teagasc Food Rearch Centre, Moorepark, Fermoy, Cork, Ireland.
