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      Lipopolysaccharide structures of Gram-negative populations in the gut microbiota and effects on host interactions

      1 , 2 , 2 , 3 , 1 , 2 , 1 , 2
      FEMS Microbiology Reviews
      Oxford University Press (OUP)

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          Abstract

          <p class="first" id="d16289520e103">The human gastrointestinal tract harbors a heterogeneous and complex microbial community, which plays a key role in human health. The gut microbiota controls the development of the immune system by setting systemic threshold for immune activation. Glycoconjugates, such as lipopolysaccharides, from gut bacteria have been shown to be able to elicit both systemic proinflammatory and immunomodulatory responses. This phenomenon is particularly intriguing considering that the immune system is charged with the task to distinguish the beneficial microbes from the pathogens, even if the commensal bacteria have molecular patterns resembling those of the pathogenic counterparts. Therefore, the importance of the chemical structure of these macromolecules in fine tuning this delicate equilibrium is beyond question. This review offers an overview of the current understanding of chemical peculiarities of the lipopolysaccharides isolated from the gut microbiota, and their relationships to their biological activity in terms of immune system maturation and development. </p>

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          Diversity of the human intestinal microbial flora.

          The human endogenous intestinal microflora is an essential "organ" in providing nourishment, regulating epithelial development, and instructing innate immunity; yet, surprisingly, basic features remain poorly described. We examined 13,355 prokaryotic ribosomal RNA gene sequences from multiple colonic mucosal sites and feces of healthy subjects to improve our understanding of gut microbial diversity. A majority of the bacterial sequences corresponded to uncultivated species and novel microorganisms. We discovered significant intersubject variability and differences between stool and mucosa community composition. Characterization of this immensely diverse ecosystem is the first step in elucidating its role in health and disease.
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            • Record: found
            • Abstract: found
            • Article: not found

            Metagenomic analysis of the human distal gut microbiome.

            The human intestinal microbiota is composed of 10(13) to 10(14) microorganisms whose collective genome ("microbiome") contains at least 100 times as many genes as our own genome. We analyzed approximately 78 million base pairs of unique DNA sequence and 2062 polymerase chain reaction-amplified 16S ribosomal DNA sequences obtained from the fecal DNAs of two healthy adults. Using metabolic function analyses of identified genes, we compared our human genome with the average content of previously sequenced microbial genomes. Our microbiome has significantly enriched metabolism of glycans, amino acids, and xenobiotics; methanogenesis; and 2-methyl-d-erythritol 4-phosphate pathway-mediated biosynthesis of vitamins and isoprenoids. Thus, humans are superorganisms whose metabolism represents an amalgamation of microbial and human attributes.
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              • Record: found
              • Abstract: found
              • Article: not found

              Fusobacterium nucleatum promotes colorectal carcinogenesis by modulating E-cadherin/β-catenin signaling via its FadA adhesin.

              Fusobacterium nucleatum (Fn) has been associated with colorectal cancer (CRC), but causality and underlying mechanisms remain to be established. We demonstrate that Fn adheres to, invades, and induces oncogenic and inflammatory responses to stimulate growth of CRC cells through its unique FadA adhesin. FadA binds to E-cadherin, activates β-catenin signaling, and differentially regulates the inflammatory and oncogenic responses. The FadA-binding site on E-cadherin is mapped to an 11-amino-acid region. A synthetic peptide derived from this region of E-cadherin abolishes FadA-induced CRC cell growth and oncogenic and inflammatory responses. The fadA gene levels in the colon tissue from patients with adenomas and adenocarcinomas are >10-100 times higher compared to normal individuals. The increased FadA expression in CRC correlates with increased expression of oncogenic and inflammatory genes. This study unveils a mechanism by which Fn can drive CRC and identifies FadA as a potential diagnostic and therapeutic target for CRC. Copyright © 2013 Elsevier Inc. All rights reserved.
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                Author and article information

                Journal
                FEMS Microbiology Reviews
                Oxford University Press (OUP)
                1574-6976
                January 15 2019
                May 01 2019
                May 2019
                January 15 2019
                May 01 2019
                May 2019
                : 43
                : 3
                : 257-272
                Affiliations
                [1 ]Department of Chemical Sciences, University of Naples Federico II, via Cinthia 4, 80126 Naples, Italy
                [2 ]Task Force on Microbiome Studies, University of Naples Federico II, via Cinthia 4, 80126 Naples, Italy
                [3 ]Department of Agricultural Sciences, University of Naples Federico II, via Università 100, 80055 Portici, Italy
                Article
                10.1093/femsre/fuz002
                30649292
                e3c76b72-a6d5-4703-8320-cc6daa7d7e23
                © 2019

                https://academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model

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