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Influence of NOD2 Variants on Trichuris suis ova Treatment Outcome in Crohn’s Disease

Jaeger, Simon U., Schaeffeler, Elke, Winter, Stefan, Tremmel, Roman, Schölmerich, Jürgen, Malek, Nisar, Stange, Eduard F., Schwab, Matthias, Wehkamp, Jan·2018·Frontiers in Pharmacology
DOI 10.3389/fphar.2018.00764PMC PMC6054957
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Crossref · 10.3389/fphar.2018.00764

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FIGURE 1 (A) Minor allele frequency in the cohort and general population, and P-value from χ2-test of Hardy–Weinberg equilibrium (HWE). ∗Data from 1000 Genomes Project (Europeans, Phase 3, build 144, http://www.internationalgenome.org/data). (B) Top: Schematic representation of the NOD2 protein, location of changes in amino acid sequence. LRR, leucine rich repeat; CARD, caspase recruitment domain; NBD, nuclear binding domain. Bottom: Graphic representation of haplotypes, sorted by frequency, as well as tabular summary of haplotype analysis result. §“Rare” haplotype summarizes all uncommon haplotypes (frequency < 5%). #Based on logistic regression analysis comparing each haplotype versus the effect of the “base” haplotype (the most common haplotype).
FIGURE 1 (A) Minor allele frequency in the cohort and general population, and P-value from χ2-test of Hardy–Weinberg equilibrium (HWE). ∗Data from 1000 Genomes Project (Europeans, Phase 3, build 144, http://www.internationalgenome.org/data). (B) Top: Schematic representation of the NOD2 protein, location of changes in amino acid sequence. LRR, leucine rich repeat; CARD, caspase recruitment domain; NBD, nuclear binding domain. Bottom: Graphic representation of haplotypes, sorted by frequency, as well as tabular summary of haplotype analysis result. §“Rare” haplotype summarizes all uncommon haplotypes (frequency < 5%). #Based on logistic regression analysis comparing each haplotype versus the effect of the “base” haplotype (the most common haplotype).CC BY · PubMed Central

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Research works printed but not linked: 19

  1. Al Nabhani, 2016, Nod2 deficiency leads to a specific and transmissible mucosa-associated microbial dysbiosis which is independent of the mucosal barrier defect., J. Crohns Colitis, 10, 1428, 10.1093/ecco-jcc/jjw095 · DOI
  2. Bowcutt, 2014, A role for the pattern recognition receptor Nod2 in promoting recruitment of CD103 + + dendritic cells to the colon in response to Trichuris muris infection., Mucosal Immunol., 7, 1094, 10.1038/mi.2013.125 · DOI
  3. Carmody, 2015, Diet dominates host genotype in shaping the murine gut microbiota., Cell Host Microbe, 17, 72, 10.1016/j.chom.2014.11.010 · DOI · Paper page
  4. Cleynen, 2016, Inherited determinants of Crohn’s disease and ulcerative colitis phenotypes: a genetic association study., Lancet, 387, 156, 10.1016/S0140-6736(15)00465-1 · DOI
  5. González, 2007, SNPassoc: an R package to perform whole genome association studies., Bioinformatics, 23, 644, 10.1093/bioinformatics/btm025 · DOI
  6. Hiemstra, 2014, Excreted/secreted Trichuris suis products reduce barrier function and suppress inflammatory cytokine production of intestinal epithelial cells., Mol. Immunol., 60, 1, 10.1016/j.molimm.2014.03.003 · DOI
  7. Hugot, 2001, Association of NOD2 leucine-rich repeat variants with susceptibility to Crohn’s disease., Nature, 411, 599, 10.1038/35079107 · DOI · Paper page
  8. Kennedy, 2018, The impact of NOD2 variants on fecal microbiota in Crohn’s disease and controls without Gastrointestinal disease., Inflamm. Bowel Dis., 24, 583, 10.1093/ibd/izx061 · DOI
  9. Nelson, 2016, The genetics of drug efficacy: opportunities and challenges., Nat. Rev. Genet., 17, 197, 10.1038/nrg.2016.12 · DOI
  10. 2017, A Language and Environment for Statistical Computing.
  11. Ramanan, 2016, Helminth infection promotes colonization resistance via type 2 immunity., Science, 352, 608, 10.1126/science.aaf3229 · DOI
  12. Sandborn, 2013, Randomised clinical trial: the safety and tolerability of Trichuris suis ova in patients with Crohn’s disease., Aliment. Pharmacol. Ther., 38, 255, 10.1111/apt.12366 · DOI
  13. Schölmerich, 2017, A randomised, double-blind, placebo-controlled trial of Trichuris suis ova in active Crohn’s disease., J. Crohns Colitis, 11, 390, 10.1093/ecco-jcc/jjw184 · DOI · Paper page
  14. Schwab, 2003, Association between the C3435T MDR1 gene polymorphism and susceptibility for ulcerative colitis., Gastroenterology, 124, 26, 10.1053/gast.2003.50010 · DOI
  15. Shanahan, 2014, Mouse Paneth cell antimicrobial function is independent of Nod2., Gut, 63, 903, 10.1136/gutjnl-2012-304190 · DOI
  16. Sinnwell, 2018, haplo.stats: Statistical Analysis of Haplotypes with Traits and Covariates when Linkage Phase is Ambiguous. R Package Version 1.7.7.
  17. Summers, Trichuris suis therapy in Crohn’s disease., Gut, 54, 87, 10.1136/gut.2004.041749 · DOI · Paper page
  18. Summers, Trichuris suis therapy for active ulcerative colitis: a randomized controlled trial., Gastroenterology, 128, 825, 10.1053/j.gastro.2005.01.005 · DOI · Paper page
  19. Wehkamp, 2004, NOD2 (CARD15) mutations in Crohn’s disease are associated with diminished mucosal alpha-defensin expression., Gut, 53, 1658, 10.1136/gut.2003.032805 · DOI

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Metadata

Authors
Jaeger, S. U., Schaeffeler, E., Winter, S., Tremmel, R., Schölmerich, J., Malek, N., Stange, E. F., Schwab, M., & Wehkamp, J.
Venue
Frontiers in Pharmacology
Publisher
Frontiers Media SA
Published
2018-07-16
Volume
9
ISSN
1663-9812
DOI
10.3389/fphar.2018.00764
PMC
PMC6054957
Cited by
3
References
2
Licence
creativecommons.org/licenses/by/4.0/ (unspecified)
Funders
  • Deutsche Forschungsgemeinschaft (Heisenberg Programme)
  • Robert Bosch Stiftung (Robert Bosch Stiftung is the founding body of Margarete Fischer-Bosch Institute of Pharmacology)

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