116
Views
20
CrossRef citations to date
0
Altmetric
Review

Mycobacteria in Crohn’s disease: how innate immune deficiency may result in chronic inflammation

&
Pages 633-641 | Published online: 10 Jan 2014

References

  • Gasche C, Scholmerich J, Brynskov J et al. A simple classification of Crohn’s disease: report of the Working Party for the World Congresses of Gastroenterology, Vienna 1998. Inflamm. Bowel Dis.6(1), 8–15 (2000).
  • Bouma G, Strober W. The immunological and genetic basis of inflammatory bowel disease. Nat. Rev. Immunol.3(7), 521–533 (2003).
  • Strober W, Fuss I, Mannon P. The fundamental basis of inflammatory bowel disease. J. Clin. Invest.117(3), 514–521 (2007).
  • Schoepfer AM, Schaffer T, Mueller S et al. Phenotypic associations of Crohn’s disease with antibodies to flagellins A4-Fla2 and Fla-X, ASCA, p-ANCA, PAB, and NOD2 mutations in a Swiss cohort. Inflamm. Bowel Dis.15(9), 1358–1367 (2009).
  • Hugot JP, Chamaillard M, Zouali H et al. Association of NOD2 leucine-rich repeat variants with susceptibility to Crohn’s disease. Nature411(6837), 599–603 (2001).
  • Hampe J, Franke A, Rosenstiel P et al. A genome-wide association scan of nonsynonymous SNPs identifies a susceptibility variant for Crohn disease in ATG16L1. Nat. Genet.39(2), 207–211 (2007).
  • Parkes M, Barrett JC, Prescott NJ et al. Sequence variants in the autophagy gene IRGM and multiple other replicating loci contribute to Crohn’s disease susceptibility. Nat. Genet.39(7), 830–832 (2007).
  • Levine B, Deretic V. Unveiling the roles of autophagy in innate and adaptive immunity. Nat. Rev. Immunol.7(10), 767–777 (2007).
  • Behr MA, Schurr E. Mycobacteria in Crohn’s disease: a persistent hypothesis. Inflamm. Bowel Dis.12(10), 1000–1004 (2006).
  • Tysk C, Lindberg E, Jarnerot G, Floderus-Myrhed B. Ulcerative colitis and Crohn’s disease in an unselected population of monozygotic and dizygotic twins. A study of heritability and the influence of smoking. Gut29(7), 990–996 (1988).
  • Cuthbert AP, Fisher SA, Mirza MM et al. The contribution of NOD2 gene mutations to the risk and site of disease in inflammatory bowel disease. Gastroenterology122(4), 867–874 (2002).
  • Barrett JC, Hansoul S, Nicolae DL et al. Genome-wide association defines more than 30 distinct susceptibility loci for Crohn’s disease. Nat. Genet.40(8), 955–962 (2008).
  • Penack O, Smith OM, Cunningham-Bussel A et al. NOD2 regulates hematopoietic cell function during graft-versus-host disease. J. Exp. Med.206(10), 2101–2110 (2009).
  • Yang Y, Yin C, Pandey A, Abbott D, Sassetti C, Kelliher MA. NOD2 pathway activation by MDP or Mycobacterium tuberculosis infection involves the stable polyubiquitination of Rip2. J. Biol. Chem.282(50), 36223–36229 (2007).
  • Kobayashi K, Inohara N, Hernandez LD et al. RICK/Rip2/CARDIAK mediates signalling for receptors of the innate and adaptive immune systems. Nature416(6877), 194–199 (2002).
  • Abbott DW, Wilkins A, Asara JM, Cantley LC. The Crohn’s disease protein, NOD2, requires RIP2 in order to induce ubiquitinylation of a novel site on NEMO. Curr. Biol.14(24), 2217–2227 (2004).
  • Kufer TA, Sansonetti PJ. Sensing of bacteria: NOD a lonely job. Curr. Opin. Microbiol.10(1), 62–69 (2007).
  • Bonen DK, Ogura Y, Nicolae DL et al. Crohn’s disease-associated NOD2 variants share a signaling defect in response to lipopolysaccharide and peptidoglycan. Gastroenterology124(1), 140–146 (2003).
  • Inohara N, Ogura Y, Fontalba A et al. Host recognition of bacterial muramyl dipeptide mediated through NOD2. Implications for Crohn’s disease. J. Biol. Chem.278(8), 5509–5512 (2003).
  • van Heel DA, Ghosh S, Butler M et al. Muramyl dipeptide and Toll-like receptor sensitivity in NOD2-associated Crohn’s disease. Lancet365(9473), 1794–1796 (2005).
  • Netea MG, Kullberg BJ, de Jong DJ et al. NOD2 mediates anti-inflammatory signals induced by TLR2 ligands: implications for Crohn’s disease. Eur. J. Immunol.34(7), 2052–2059 (2004).
  • Adam A, Petit JF, Wietzerbin-Falszpan J Sinay P, Thomas DW, Lederer E. [No title available]. FEBS Lett.4(2), 87–92 (1969).
  • Raymond JB, Mahapatra S, Crick DC, Pavelka MS Jr. Identification of the namH gene, encoding the hydroxylase responsible for the N-glycolylation of the mycobacterial peptidoglycan. J. Biol. Chem.280(1), 326–333 (2005).
  • Schleifer KH, Kandler O. Peptidoglycan types of bacterial cell walls and their taxonomic implications. Bacteriol. Rev.36(4), 407–477 (1972).
  • Lederer E, Adam A, Ciorbaru R, Petit JF, Wietzerbin J. Cell walls of Mycobacteria and related organisms; chemistry and immunostimulant properties. Mol. Cell. Biochem.7(2), 87–104 (1975).
  • Freund J. The mode of action of immunologic adjuvants. Bibl. Tuberc.7(10), 130–148 (1956).
  • Ferwerda G, Girardin SE, Kullberg BJ et al. NOD2 and Toll-like receptors are nonredundant recognition systems of Mycobacterium tuberculosis. PLoS Pathog.1(3), 279–285 (2005).
  • Ferwerda G, Kullberg BJ, de Jong DJ et al.Mycobacterium paratuberculosis is recognized by Toll-like receptors and NOD2. J. Leukoc. Biol.82(4), 1011–1018 (2007).
  • Divangahi M, Mostowy S, Coulombe F et al. NOD2-deficient mice have impaired resistance to Mycobacterium tuberculosis infection through defective innate and adaptive immunity. J. Immunol.181(10), 7157–7165 (2008).
  • Coulombe F, Divangahi M, Veyrier F et al. Increased NOD2-mediated recognition of N-glycolyl muramyl dipeptide. J. Exp. Med.206(8), 1709–1716 (2009).
  • Pandey AK, Yang Y, Jiang Z et al. NOD2, RIP2 and IRF5 play a critical role in the type I interferon response to Mycobacterium tuberculosis. PLoS Pathog.5(7), e1000500 (2009).
  • Travassos LH, Carneiro LA, Ramjeet M et al. Nod1 and Nod2 direct autophagy by recruiting ATG16L1 to the plasma membrane at the site of bacterial entry. Nat. Immunol.11(1), 55–62 (2009).
  • Cooney R, Baker J, Brain O et al. NOD2 stimulation induces autophagy in dendritic cells influencing bacterial handling and antigen presentation. Nat. Med.16(1), 90–97 (2009).
  • MacMicking JD, Taylor GA, McKinney JD. Immune control of tuberculosis by IFN-γ-inducible LRG-47. Science302(5645), 654–659 (2003).
  • Feng CG, Collazo-Custodio CM, Eckhaus M et al. Mice deficient in LRG-47 display increased susceptibility to mycobacterial infection associated with the induction of lymphopenia. J. Immunol.172(2), 1163–1168 (2004).
  • Marciano BE, Rosenzweig SD, Kleiner DE et al. Gastrointestinal involvement in chronic granulomatous disease. Pediatrics114(2), 462–468 (2004).
  • Daniels JA, Lederman HM, Maitra A, Montgomery EA. Gastrointestinal tract pathology in patients with common variable immunodeficiency (CVID): a clinicopathologic study and review. Am. J. Surg. Pathol.31(12), 1800–1812 (2007).
  • Dieckgraefe BK, Korzenik JR, Husain A, Dieruf L. Association of glycogen storage disease 1b and Crohn disease: results of a North American survey. Eur. J. Pediatr.161(Suppl. 1), S88–S92 (2002).
  • Kuramoto S, Oohara T, Ihara O, Shimazu R, Kondo Y. Granulomas of the gut in Crohn’s disease. A step sectioning study. Dis. Colon Rectum30(1), 6–11 (1987).
  • Marks DJ, Harbord MW, MacAllister R et al. Defective acute inflammation in Crohn’s disease: a clinical investigation. Lancet367(9511), 668–678 (2006).
  • Smith AM, Rahman FZ, Hayee B et al. Disordered macrophage cytokine secretion underlies impaired acute inflammation and bacterial clearance in Crohn’s disease. J. Exp. Med.206(9), 1883–1897 (2009).
  • Seidelin JB, Broom OJ, Olsen J, Nielsen OH. Evidence for impaired CARD15 signalling in Crohn’s disease without disease linked variants. PLoS One4(11), e7794 (2009).
  • Casanova JL, Abel L. Revisiting Crohn’s disease as a primary immunodeficiency of macrophages. J. Exp. Med.206(9), 1839–1843 (2009).
  • Behr MA. The path to Crohn’s disease: is mucosal pathology a secondary event? Inflamm. Bowel Dis.16(5), 896–902 (2009).
  • Hansen R, Thomson JM, El-Omar EM, Hold GL. The role of infection in the aetiology of inflammatory bowel disease. J. Gastroenterol.45(3), 266–276 (2010).
  • Hines ME 2nd, Stabel JR, Sweeney RW et al. Experimental challenge models for Johne’s disease: a review and proposed international guidelines. Vet. Microbiol.122(3–4), 197–222 (2007).
  • Greenstein RJ. Is Crohn’s disease caused by a mycobacterium? Comparisons with leprosy, tuberculosis, and Johne’s disease. Lancet Infect. Dis.3(8), 507–514 (2003).
  • Chacon O, Bermudez LE, Barletta RG. Johne’s disease, inflammatory bowel disease, and Mycobacterium paratuberculosis. Annu. Rev. Microbiol.58, 329–363 (2004).
  • Van Kruiningen HJ. Lack of support for a common etiology in Johne’s disease of animals and Crohn’s disease in humans. Inflamm. Bowel Dis.5(3), 183–191 (1999).
  • Dalziel T. Chronic interstitial enteritis. BMJ2, 1068–1070 (1913).
  • Greig A, Stevenson K, Henderson D et al. Epidemiological study of paratuberculosis in wild rabbits in Scotland. J. Clin. Microbiol.37(6), 1746–1751 (1999).
  • McClure HM, Chiodini RJ, Anderson DC, Swenson RB, Thayer WR, Coutu JA. Mycobacterium paratuberculosis infection in a colony of stumptail macaques (Macaca arctoides). J. Infect. Dis.155(5), 1011–1019 (1987).
  • Abubakar I, Myhill D, Aliyu SH, Hunter PR. Detection of Mycobacterium avium subspecies paratuberculosis from patients with Crohn’s disease using nucleic acid-based techniques: a systematic review and meta-analysis. Inflamm. Bowel Dis.14(3), 401–410 (2008).
  • Feller M, Huwiler K, Stephan R et al.Mycobacterium avium subspecies paratuberculosis and Crohn’s disease: a systematic review and meta-analysis. Lancet Infect. Dis.7(9), 607–613 (2007).
  • Austin CM, Ma X, Graviss EA. Common nonsynonymous polymorphisms in the NOD2 gene are associated with resistance or susceptibility to tuberculosis disease in African Americans. J. Infect. Dis.197(12), 1713–1716 (2008).
  • Pinedo PJ, Buergelt CD, Donovan GA et al. Association between CARD15/NOD2 gene polymorphisms and paratuberculosis infection in cattle. Vet. Microbiol.134(3–4), 346–352 (2009).
  • Zhang FR, Huang W, Chen SM et al. Genomewide association study of leprosy. N. Engl. J. Med.361(27), 2609–2618 (2009).
  • Berrington WR, Macdonald M, Khadge S et al. Common polymorphisms in the NOD2 gene region are associated with leprosy and its reactive states. J. Infect. Dis.201(9), 1422–1435 (2010).
  • Pulimood AB, Ramakrishna BS, Kurian G et al. Endoscopic mucosal biopsies are useful in distinguishing granulomatous colitis due to Crohn’s disease from tuberculosis. Gut45(4), 537–541 (1999).
  • Sibartie S, Scully P, Keohane J et al.Mycobacterium avium subsp. paratuberculosis (MAP) as a modifying factor in Crohn’s disease. Inflamm. Bowel Dis.16(2), 296–304 (2010).
  • Olsen I, Tollefsen S, Aagaard C et al. Isolation of Mycobacterium avium subspecies paratuberculosis reactive CD4 T cells from intestinal biopsies of Crohn’s disease patients. PLoS One4(5), e5641 (2009).
  • Selby W, Pavli P, Crotty B et al. Two-year combination antibiotic therapy with clarithromycin, rifabutin, and clofazimine for Crohn’s disease. Gastroenterology132(7), 2313–2319 (2007).
  • Behr MA, Hanley J. Antimycobacterial therapy for Crohn’s disease: a reanalysis. Lancet Infect. Dis.8(6), 344 (2008).
  • Gui GP, Thomas PR, Tizard ML, Lake J, Sanderson JD, Hermon-Taylor J. Two-year-outcomes analysis of Crohn’s disease treated with rifabutin and macrolide antibiotics. J. Antimicrob. Chemother.39(3), 393–400 (1997).
  • Feller M, Huwiler K, Schoepfer A, Shang A, Furrer H, Egger M. Long-term antibiotic treatment for Crohn’s disease: systematic review and meta-analysis of placebo-controlled trials. Clin. Infect. Dis.50(4), 473–480 (2010).
  • Behr MA, Kapur V. The evidence for Mycobacterium paratuberculosis in Crohn’s disease. Curr. Opin. Gastroenterol.24(1), 17–21 (2008).
  • Kuballa P, Huett A, Rioux JD, Daly MJ, Xavier RJ. Impaired autophagy of an intracellular pathogen induced by a Crohn’s disease associated ATG16L1 variant. PLoS One3(10), e3391 (2008).
  • Singh SB, Davis AS, Taylor GA, Deretic V. Human IRGM induces autophagy to eliminate intracellular mycobacteria. Science313(5792), 1438–1441 (2006).
  • Hsu YH, Chen CW, Sun HS, Jou R, Lee JJ, Su IJ. Association of NRAMP1 gene polymorphism with susceptibility to tuberculosis in Taiwanese aboriginals. J. Formos. Med. Assoc.105(5), 363–369 (2006).
  • Van Limbergen J, Wilson DC, Satsangi J. The genetics of Crohn’s disease. Annu. Rev. Genomics Hum. Genet.10, 89–116 (2009).
  • Abel L, Sanchez FO, Oberti J et al. Susceptibility to leprosy is linked to the human NRAMP1 gene. J. Infect. Dis.177(1), 133–145 (1998).
  • Gao L, Tao Y, Zhang L, Jin Q. Vitamin D receptor genetic polymorphisms and tuberculosis: updated systematic review and meta-analysis. Int. J. Tuberc. Lung Dis.14(1), 15–23 (2010).
  • Behr MA. Mycobacterium du jour: what’s on tomorrow’s menu? Microbes Infect.10(9), 968–972 (2008).
  • Diagnosis and treatment of disease caused by nontuberculous mycobacteria. This official statement of the American Thoracic Society was approved by the Board of Directors, March 1997. Medical Section of the American Lung Association. Am. J. Respir. Crit. Care. Med.156(2 Pt 2), S1–S25 (1997).
  • Turenne CY, Collins DM, Alexander DC, Behr MA. Mycobacterium avium subsp. paratuberculosis and M. avium subsp. avium are independently evolved pathogenic clones of a much broader group of M. avium organisms. J. Bacteriol.190(7), 2479–2487 (2008).
  • Thoma-Uszynski S, Stenger S, Takeuchi O et al. Induction of direct antimicrobial activity through mammalian Toll-like receptors. Science291(5508), 1544–1547 (2001).
  • Ishikawa E, Ishikawa T, Morita YS et al. Direct recognition of the mycobacterial glycolipid, trehalose dimycolate, by C-type lectin Mincle. J. Exp. Med.206(13), 2879–2888 (2009).
  • Walburger A, Koul A, Ferrari G et al. Protein kinase G from pathogenic mycobacteria promotes survival within macrophages. Science304(5678), 1800–1804 (2004).
  • Reed MB, Domenech P, Manca C et al. A glycolipid of hypervirulent tuberculosis strains that inhibits the innate immune response. Nature431(7004), 84–87 (2004).
  • Gutierrez MG, Master SS, Singh SB, Taylor GA, Colombo MI, Deretic V. Autophagy is a defense mechanism inhibiting BCG and Mycobacterium tuberculosis survival in infected macrophages. Cell119(6), 753–766 (2004).
  • Kumar D, Nath L, Kamal MA et al. Genome-wide analysis of the host intracellular network that regulates survival of Mycobacterium tuberculosis. Cell140(5), 731–743 (2010).
  • Divangahi M, Chen M, Gan H et al.Mycobacterium tuberculosis evades macrophage defenses by inhibiting plasma membrane repair. Nat. Immunol.10(8), 899–906 (2009).
  • Tobin DM, Vary JC Jr, Ray JP et al. The lta4h locus modulates susceptibility to mycobacterial infection in zebrafish and humans. Cell140(5), 717–730 (2010).
  • Behr M, Schurr E, Gros P. TB: screening for responses to a vile visitor. Cell140(5), 615–618 (2010).
  • Henry SC, Daniell X, Indaram M et al. Impaired macrophage function underscores susceptibility to Salmonella in mice lacking Irgm1 (LRG-47). J. Immunol.179(10), 6963–6972 (2007).
  • Collazo CM, Yap GS, Sempowski GD et al. Inactivation of LRG-47 and IRG-47 reveals a family of interferon g-inducible genes with essential, pathogen-specific roles in resistance to infection. J. Exp. Med.194(2), 181–188 (2001).
  • Santiago HC, Feng CG, Bafica A et al. Mice deficient in LRG-47 display enhanced susceptibility to Trypanosoma cruzi infection associated with defective hemopoiesis and intracellular control of parasite growth. J. Immunol.175(12), 8165–8172 (2005).

Reprints and Corporate Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

To request a reprint or corporate permissions for this article, please click on the relevant link below:

Academic Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

Obtain permissions instantly via Rightslink by clicking on the button below:

If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.