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      The vesicle-associated function of NOD2 as a link between Crohn’s disease and mycobacterial infection

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      Author(s):
      Publication date (Electronic):
      Journal: Gut Pathogens
      Publisher: BioMed Central
      Keywords: Vesicle acidity, Crohn’s disease, Mycobacteria, Sulfonated glycolipids, Autophagy, Pattern recognition receptors

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          Abstract

          Although Crohn’s disease (CD) etiology remains unclear, a growing body of evidence suggests that CD may include an infectious component, with Mycobacterium avium subsp. paratuberculosis (MAP) being the most likely candidate for this role. However, the molecular mechanism of the MAP involvement in CD pathogenesis remains unclear. The polymorphism of the NOD2 gene, coding for an intracellular pattern recognition receptor, is a factor of predisposition to mycobacterial infections and CD. Recent findings on NOD2 interactions and functions provide the missing pieces in the puzzle of a NOD2-mediated mechanism common for mycobacterial infections and CD. Implications of these new findings for the development of a better understanding and treatments of CD and mycobacterial infections are discussed.

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          Association of NOD2 leucine-rich repeat variants with susceptibility to Crohn's disease.

          J Hugot, M Chamaillard, H Zouali … (2001)
          Crohn's disease and ulcerative colitis, the two main types of chronic inflammatory bowel disease, are multifactorial conditions of unknown aetiology. A susceptibility locus for Crohn's disease has been mapped to chromosome 16. Here we have used a positional-cloning strategy, based on linkage analysis followed by linkage disequilibrium mapping, to identify three independent associations for Crohn's disease: a frameshift variant and two missense variants of NOD2, encoding a member of the Apaf-1/Ced-4 superfamily of apoptosis regulators that is expressed in monocytes. These NOD2 variants alter the structure of either the leucine-rich repeat domain of the protein or the adjacent region. NOD2 activates nuclear factor NF-kB; this activating function is regulated by the carboxy-terminal leucine-rich repeat domain, which has an inhibitory role and also acts as an intracellular receptor for components of microbial pathogens. These observations suggest that the NOD2 gene product confers susceptibility to Crohn's disease by altering the recognition of these components and/or by over-activating NF-kB in monocytes, thus documenting a molecular model for the pathogenic mechanism of Crohn's disease that can now be further investigated.
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            Genomewide association study of leprosy.

            Fu-Ren Zhang, Wei Huang, Shu-Min Chen … (2009)
            The narrow host range of Mycobacterium leprae and the fact that it is refractory to growth in culture has limited research on and the biologic understanding of leprosy. Host genetic factors are thought to influence susceptibility to infection as well as disease progression. We performed a two-stage genomewide association study by genotyping 706 patients and 1225 controls using the Human610-Quad BeadChip (Illumina). We then tested three independent replication sets for an association between the presence of leprosy and 93 single-nucleotide polymorphisms (SNPs) that were most strongly associated with the disease in the genomewide association study. Together, these replication sets comprised 3254 patients and 5955 controls. We also carried out tests of heterogeneity of the associations (or lack thereof) between these 93 SNPs and disease, stratified according to clinical subtype (multibacillary vs. paucibacillary). We observed a significant association (P<1.00x10(-10)) between SNPs in the genes CCDC122, C13orf31, NOD2, TNFSF15, HLA-DR, and RIPK2 and a trend toward an association (P=5.10x10(-5)) with a SNP in LRRK2. The associations between the SNPs in C13orf31, LRRK2, NOD2, and RIPK2 and multibacillary leprosy were stronger than the associations between these SNPs and paucibacillary leprosy. Variants of genes in the NOD2-mediated signaling pathway (which regulates the innate immune response) are associated with susceptibility to infection with M. leprae. 2009 Massachusetts Medical Society
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              5-Hydroxytryptamine (serotonin) in the gastrointestinal tract.

              Michael D Gershon (2013)
              Although the gut contains most of the body's 5-hydroxytryptamine (5-HT), many of its most important functions have recently been discovered. This review summarizes and directs attention to this new burst of knowledge. Enteroendocrine cells have classically been regarded as pressure sensors, which secrete 5-HT to initiate peristaltic reflexes; nevertheless, recent data obtained from studies of mice that selectively lack 5-HT either in enterochromaffin cells (deletion of tryptophan hydroxylase 1 knockout; TPH1KO) or neurons (TPH2KO) imply that neuronal 5-HT is more important for constitutive gastrointestinal transit than that of enteroendocrine cells. The enteric nervous system of TPH2KO mice, however, also lacks a full complement of neurons; therefore, it is not clear whether slow transit in TPH2KO animals is due to their neuronal deficiency or absence of serotonergic neurotransmission. Neuronal 5-HT promotes the growth/maintenance of the mucosa as well as neurogenesis. Enteroendocrine cell derived 5-HT is an essential component of the gastrointestinal inflammatory response; thus, deletion of the serotonin transporter increases, whereas TPH1KO decreases the severity of intestinal inflammation. Enteroendocrine cell derived 5-HT, moreover, is also a hormone, which inhibits osteoblast proliferation and promotes hepatic regeneration. New studies show that enteric 5-HT is a polyfunctional signalling molecule, acting both in developing and mature animals as a neurotransmitter paracrine factor, endocrine hormone and growth factor.
              Article 0 comments Cited 212 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Alexey A Nabatov: alexey.nabatov@maastrichtuniversity.nl
                Journal
                Journal ID (nlm-ta): Gut Pathog
                Journal ID (iso-abbrev): Gut Pathog
                Title: Gut Pathogens
                Publisher: BioMed Central (London )
                ISSN (Electronic): 1757-4749
                Publication date (Electronic): 29 January 2015
                Publication date PMC-release: 29 January 2015
                Publication date Collection: 2015
                Volume: 7
                Issue: 1
                Electronic Location Identifier: 1
                Affiliations
                [ ]Maastricht Radiation Oncology, MAASTRO/GROW Maastricht University Medical Center+, PO Box 616, 6200 MD Maastricht, The Netherlands
                [ ]Science Center, Volga Region State Academy of Physical Culture, Sport and Tourism, 33, Universiade Village, Kazan, 420138 Russia
                Article
                Publisher ID: 49
                DOI: 10.1186/s13099-015-0049-1
                PMC ID: 4316803
                PubMed ID: 25653718
                SO-VID: 63795bf1-ab26-4ff7-b7cd-2e24e9056c0c
                Copyright © © Nabatov; licensee BioMed Central. 2015
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                Date received : 24 October 2014
                Date accepted : 3 January 2015
                Categories
                Subject: Review
                Custom metadata
                issue-copyright-statement © The Author(s) 2015

                ScienceOpen disciplines: Gastroenterology & Hepatology
                Keywords: vesicle acidity,crohn’s disease,mycobacteria,sulfonated glycolipids,autophagy,pattern recognition receptors
                Data availability:
                ScienceOpen disciplines: Gastroenterology & Hepatology
                Keywords: vesicle acidity, crohn’s disease, mycobacteria, sulfonated glycolipids, autophagy, pattern recognition receptors

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