621 results match your criteria Crohn's Disease and NOD2 CARD15


Single Nucleotide Polymorphisms in Selected Genes in Inflammatory Bowel Disease.

Biomed Res Int 2018 17;2018:6914346. Epub 2018 Dec 17.

Chair of Medical Genetics, Department of Clinical Genetics, Medical University of Lublin, 20-080 Lublin, Poland.

Introduction: Inflammatory bowel disease (IBD) is a complicated, multifunctional disorder characterized by chronic, recurring inflammation of the digestive tract. The two main types of IBD are ulcerative colitis (UC) and Crohn's disease (CD). The aim of the study was to determine single nucleotide polymorphism in fragments of the genes and in patients from the Lublin Voivodeship. Read More

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http://dx.doi.org/10.1155/2018/6914346DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6311883PMC
December 2018
4 Reads

NOD2/CARD15 Mutations among Bedouin Arabs with Inflammatory Bowel Disease: Frequency and Phenotype Correlation.

Isr Med Assoc J 2018 Nov;20(11):695-699

Department of Internal Medicine C, Rambam Medical Center, Technion-Israel Institute of Technology, Haifa, Israel.

Background: Inflammatory bowel disease (IBD) prevalence is increasing among Bedouin Arabs in Israel. This population is known to have a high rate of consanguinity. NOD2/CARD15 mutations are well-studied in IBD. Read More

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November 2018
16 Reads
0.903 Impact Factor

CTLA-4 (+49A/G) and NOD2/CARD15 (N852S) polymorphisms with inflammatory bowel disease in Turkish patients.

Cell Mol Biol (Noisy-le-grand) 2018 Aug 30;64(11):97-101. Epub 2018 Aug 30.

Department of Gastroenterology, Faculty of Medicine, University of Mersin, Mersin, Turkey.

Crohn's disease (CD) and ulcerative colitis (UC) are the major types of inflammatory bowel disease (IBD) and exhibit similar clinical features and epidemiology. The main objective of this study was to analyze the correlation between the CTLA-4 gene +49A/G polymorphism and the NOD2/CARD15 gene N852S polymorphism in Turkish patients with IBD using polymerase chain reaction and restriction fragment length polymorphism (PCR-RFLP) analysis. In this study, we evaluated the frequency of the CTLA-4 (+49A/G) and NOD2/CARD15 (N852S) polymorphisms in 62 patients with CD, 76 patients with UC, and 152 healthy individuals. Read More

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August 2018
5 Reads

The role of the NOD2/CARD15 gene in surgical treatment prediction in patients with Crohn's disease.

Int J Colorectal Dis 2019 Feb 2;34(2):347-351. Epub 2018 Aug 2.

Department of Surgery, University Hospital Brno Bohunice, Faculty of Medicine, Masaryk University, Jihlavska 20, 62500, Brno, Czech Republic.

Purpose: Crohn's disease (CD) belongs to chronic disorders with unpredictable disease course. The aim of this study was to identify how genetic testing (NOD2/CARD15) can be used in patients with CD to predict the need for surgical treatment (to define an aggressive type of disease where the patient can profit from early surgery).

Methods: The patients who were tested genetically had undergone a surgery due to CD at the Department of Surgery University Hospital Brno Bohunice between 2010 and 2016. Read More

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http://dx.doi.org/10.1007/s00384-018-3122-7DOI Listing
February 2019
6 Reads

Genetic deficiency of NOD2 confers resistance to invasive aspergillosis.

Nat Commun 2018 07 6;9(1):2636. Epub 2018 Jul 6.

Department of Experimental Internal Medicine and Radboud Center for Infectious Diseases (RCI), Radboud University Medical Center, Geert Grooteplein zuid 8, 6525GA, Nijmegen, The Netherlands.

Invasive aspergillosis (IA) is a severe infection that can occur in severely immunocompromised patients. Efficient immune recognition of Aspergillus is crucial to protect against infection, and previous studies suggested a role for NOD2 in this process. However, thorough investigation of the impact of NOD2 on susceptibility to aspergillosis is lacking. Read More

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http://dx.doi.org/10.1038/s41467-018-04912-3DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6035256PMC
July 2018
9 Reads

Crohn's disease - genetic factors and progress of the disease.

Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub 2018 Jun 18;162(2):139-143. Epub 2018 Jan 18.

Department of Internal Medicine, University Hospital Ostrava, Czech Republic.

Background And Objectives: Crohn's disease is a multifactorial inflammatory disease affecting mainly the gastrointestinal tract. The genetic factors that are involved in the disease include mainly three mutations of the gene NOD2/CARD15 (R702W, G908R, 3020insC). The aim of this study was to determine the relationship between the presence of these variants and disease phenotype. Read More

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http://dx.doi.org/10.5507/bp.2017.058DOI Listing
June 2018
5 Reads

Genetic association and phenotypic correlation of TLR4 but not NOD2 variants with Tunisian inflammatory bowel disease.

J Dig Dis 2017 Nov;18(11):625-633

Department of Immunology, Habib Bourguiba University Hospital, Sfax, Tunisia.

Objective: The common association between NOD2/CARD15 and TLR4 gene variants with inflammatory bowel disease (IBD) has not been replicated in all studies. We studied the polymorphism of these two genes in Tunisian patients with IBD.

Methods: Polymorphisms of NOD2 (R702W, G908R and L1007fs) and TLR4 (Asp299Gly and Thr399Ile) genes were analyzed in 106 patients with IBD (68 with ulcerative colitis [UC], 38 with Crohn's disease [CD]) and 160 healthy controls using polymerase chain reaction-restriction fragment length polymorphism. Read More

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http://dx.doi.org/10.1111/1751-2980.12552DOI Listing
November 2017
19 Reads

[NOD2 gene mutation in Moroccan patients with Crohn's disease: prevalence, genotypic study and correlation of NOD2 gene mutation with the phenotype of Crohn's disease].

Pan Afr Med J 2017 14;27:116. Epub 2017 Jun 14.

Service d'Hépato-Gastroentérologie «B», Centre Hospitalier Universitaire Ibn Sina, Rabat, Maroc.

The aim of this study was to determine the prevalence of NOD2/CARD15 gene mutations in a group of Moroccan patients with Crohn's disease and to study its correlation with genotype-phenotypic expression. We conducted a cross-sectional case-control study over a period of 16 months. 101 patients with Crohn's disease were enrolled between January 2012 and April 2013 as well as a control group of 107 patients. Read More

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http://dx.doi.org/10.11604/pamj.2017.27.116.9187DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5554695PMC
September 2017
32 Reads

Prognostic factors affecting outcomes in fistulating perianal Crohn's disease: a systematic review.

Tech Coloproctol 2017 Jul 20;21(7):501-519. Epub 2017 Jun 20.

Department of General Surgery, Northern General Hospital, Herries Road, Sheffield, S5 7AU, UK.

Background: One in three patients with Crohn's disease will develop a perianal fistulae, and one third of these will achieve long-term healing or closure. A barrier to conducting well-designed clinical trials for these patients is a lack of understanding of prognostic factors. This systematic review sets out to identify factors associated with prognosis of perianal Crohn's fistulae. Read More

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http://dx.doi.org/10.1007/s10151-017-1647-3DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5550543PMC
July 2017
3 Reads

Complementary Roles of Nod2 in Hematopoietic and Nonhematopoietic Cells in Preventing Gut Barrier Dysfunction Dependent on MLCK Activity.

Inflamm Bowel Dis 2017 07;23(7):1109-1119

*Laboratoire d'excellence Inflamex, Université Paris-Diderot Sorbonne Paris-Cité, UMR 1149, Paris, France; †INSERM, UMR 1149, Paris, France; ‡INSERM, UMR 989, Paris, France; §Université Paris Descartes-Sorbonne Paris Cité, Institut IMAGINE, Paris, France; ‖Assistance Publique Hôpitaux de Paris, Services des Maladies Digestives et Respiratoires de l'Enfant et Service d'Anatomie Pathologique, Hôpital Robert Debré, Paris, France; and ¶Institut de Recherche en Santé Digestive IRSD, Université de Toulouse, INSERM, INRA, ENVT, UPS, 31024 Toulouse, France.

Background: Crohn's disease (CD) pathogenesis is multifactorial involving genetic and environmental factors. Loss of function mutations in the nucleotide oligomerization domain 2 (NOD2) gene are the main genetic risk factor for CD. Like patients with CD, Nod2 mice are characterized by an enhanced Th1 immune response and a defective mucosal barrier function evidenced by increased intestinal permeability. Read More

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http://dx.doi.org/10.1097/MIB.0000000000001135DOI Listing
July 2017
30 Reads

Rip2 Is Required for Nod2-Mediated Lysozyme Sorting in Paneth Cells.

J Immunol 2017 05 22;198(9):3729-3736. Epub 2017 Mar 22.

Key Laboratory of Infection and Immunity, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China;

Paneth cells play an important role in maintaining intestinal homeostasis by secreting a large number of antimicrobial peptides into the intestinal lumen. In this study, we found that Rip2 is required for lysozyme sorting in Paneth cells in a manner that is dependent on Nod2, LRRK2, and Rab2a. Rip2 deficiency in mouse led to lysosomal degradation of lysozyme in Paneth cells and prevented the recruitment of Rab2a onto dense core vesicles (DCVs). Read More

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http://dx.doi.org/10.4049/jimmunol.1601583DOI Listing
May 2017
13 Reads

Intestinal Bacteria Composition and Translocation of Bacteria in Inflammatory Bowel Disease.

PLoS One 2017 18;12(1):e0170034. Epub 2017 Jan 18.

Department of Basic Medical Sciences, Laboratory of Biology, Medical School, National and Kapodistrian University of Athens, Athens, Greece.

Background: Live commensal intestinal bacteria are present in the peripheral blood where they can induce inflammation.

Objective: To evaluate the intestinal bacteria composition and translocation of bacteria in IBD.

Methods: Both blood and tissue biopsy samples were collected from adult patients with active/inactive Crohn's disease (CD), active/inactive ulcerative colitis (UC) and healthy individuals. Read More

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http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0170034PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5242456PMC
August 2017
7 Reads

Genetic deletion of the bacterial sensor NOD2 improves murine Crohn's disease-like ileitis independent of functional dysbiosis.

Mucosal Immunol 2017 07 16;10(4):971-982. Epub 2016 Nov 16.

Department of Medicine, Case Western Reserve University, Cleveland, Ohio, USA.

Although genetic polymorphisms in NOD2 (nucleotide-binding oligomerization domain-containing 2) have been associated with the pathogenesis of Crohn's disease (CD), little is known regarding the role of wild-type (WT) NOD2 in the gut. To date, most murine studies addressing the role of WT Nod2 have been conducted using healthy (ileitis/colitis-free) mouse strains. Here, we evaluated the effects of Nod2 deletion in a murine model of spontaneous ileitis, i. Read More

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http://dx.doi.org/10.1038/mi.2016.98DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5433921PMC
July 2017
7 Reads

LRRK2 enhances Nod1/2-mediated inflammatory cytokine production by promoting Rip2 phosphorylation.

Protein Cell 2017 Jan 9;8(1):55-66. Epub 2016 Nov 9.

Key Laboratory of Infection and Immunity of CAS, Institute of Biophysics, Chinese Academy of Sciences, Beijing, 100101, China.

The innate immune system is critical for clearing infection, and is tightly regulated to avert excessive tissue damage. Nod1/2-Rip2 signaling, which is essential for initiating the innate immune response to bacterial infection and ER stress, is subject to many regulatory mechanisms. In this study, we found that LRRK2, encoded by a gene implicated in Crohn's disease, leprosy and familial Parkinson's disease, modulates the strength of Nod1/2-Rip2 signaling by enhancing Rip2 phosphorylation. Read More

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http://dx.doi.org/10.1007/s13238-016-0326-xDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5233611PMC
January 2017
13 Reads

Impact of NOD2/CARD15 polymorphisms on response to monoclonal antibody therapy in Crohn's disease: a systematic review and meta-analysis.

Curr Med Res Opin 2016 12 16;32(12):2007-2012. Epub 2016 Sep 16.

b Tongji University School of Medicine , Shanghai , China.

Objective: Crohn's disease (CD) is frequently treated with anti-tumor necrosis factor (TNF)α monoclonal antibodies, and NOD2/CARD15 polymorphisms have been reported to predict treatment response. The purpose of this study was to perform a meta-analysis to determine the effect of NOD2/CARD15 polymorphisms on treatment response in patients with CD.

Methods: Medline, Cochrane, EMBASE, and Google Scholar databases were searched until 19 December 2015 using the keywords: NOD2, CARD15, polymorphism, Crohn's disease. Read More

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http://dx.doi.org/10.1080/03007995.2016.1226168DOI Listing
December 2016
11 Reads

Nod2 Deficiency Leads to a Specific and Transmissible Mucosa-associated Microbial Dysbiosis Which Is Independent of the Mucosal Barrier Defect.

J Crohns Colitis 2016 Dec 4;10(12):1428-1436. Epub 2016 May 4.

Laboratoire d'excellence Inflamex, Université Paris-Diderot Sorbonne Paris-Cité, France

Background And Aims: Crohn's disease [CD] is a complex disorder characterised by an inappropriate immune response, impaired barrier function and microbial dysbiosis. Mutations in nucleotide oligomeriation domain 2 [NOD2] are CD risk factors. Increase of intestinal permeability, CD4 T cell infiltration, and bacterial dysbiosis are also seen in Nod2-knockout [Nod2 ] mice. Read More

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http://dx.doi.org/10.1093/ecco-jcc/jjw095DOI Listing
December 2016
23 Reads

Common NOD2/CARD15 and TLR4 Polymorphisms Are Associated with Crohn's Disease Phenotypes in Southeastern Brazilians.

Dig Dis Sci 2016 09 23;61(9):2636-47. Epub 2016 Apr 23.

Serviço de Gastroenterologia, Departamento de Clínica Médica, Hospital Universitário Clementino Fraga Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro, 21941-913, Brazil.

Aim: To investigate whether variants in NOD2/CARD15 and TLR4 are associated with CD and ulcerative colitis (UC) in a genetically admixed population of Rio de Janeiro, where IBD has continued to rise.

Methods: We recruited 67 consecutive patients with CD, 61 patients with UC, and 86 healthy and ethnically matched individuals as controls. DNA was extracted from buccal brush samples and genotyped by PCR with restriction enzymes for G908R and L1007finsC NOD2/CARD15 single-nucleotide polymorphisms (SNPs) and for T399I and D299G TLR4 SNPs. Read More

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http://dx.doi.org/10.1007/s10620-016-4172-8DOI Listing
September 2016
22 Reads

Resilience of the intestinal microbiota following pathogenic bacterial infection is independent of innate immunity mediated by NOD1 or NOD2.

Microbes Infect 2016 Jul-Aug;18(7-8):460-71. Epub 2016 Apr 12.

Department of Immunology, University of Toronto, Toronto, Ontario, M5S 1A8, Canada. Electronic address:

The innate immune receptors, NOD1 and NOD2, are key regulators of intestinal homeostasis. NOD2 deficiency is linked to increased risk for Crohn's disease, a type of inflammatory bowel disease characterized by chronic inflammatory pathology and dysbiosis within resident microbial communities. However, the relationship between NOD protein-regulated immune functions and dysbiosis remains unclear. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S12864579163002
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http://dx.doi.org/10.1016/j.micinf.2016.03.014DOI Listing
May 2017
7 Reads

Melkersson-Rosenthal Syndrome with Genitalia Involved in a 12-Year-Old Boy.

Ann Dermatol 2016 Apr 31;28(2):232-6. Epub 2016 Mar 31.

Department of Dermatology, Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.

Melkersson-Rosenthal syndrome (MRS) is an uncommon granulomatous disease characterized by the triad of relapsing facial paralysis, orofacial swelling, and fissured tongue. Genital swelling in MRS is rarely reported. We presented the first case of complete MRS with genital swelling in a child. Read More

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http://dx.doi.org/10.5021/ad.2016.28.2.232DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4828388PMC
April 2016
8 Reads

Helminth infection promotes colonization resistance via type 2 immunity.

Science 2016 Apr 14;352(6285):608-12. Epub 2016 Apr 14.

Kimmel Center for Biology and Medicine at the Skirball Institute, New York University School of Medicine, New York, NY 10016, USA. Departments of Microbiology and Medicine, New York University School of Medicine, New York, NY 10016, USA.

Increasing incidence of inflammatory bowel diseases, such as Crohn's disease, in developed nations is associated with changes to the microbial environment, such as decreased prevalence of helminth colonization and alterations to the gut microbiota. We find that helminth infection protects mice deficient in the Crohn's disease susceptibility gene Nod2 from intestinal abnormalities by inhibiting colonization by an inflammatory Bacteroides species. Resistance to Bacteroides colonization was dependent on type 2 immunity, which promoted the establishment of a protective microbiota enriched in Clostridiales. Read More

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http://dx.doi.org/10.1126/science.aaf3229DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4905769PMC
April 2016
65 Reads

Respective Roles of Hematopoietic and Nonhematopoietic Nod2 on the Gut Microbiota and Mucosal Homeostasis.

Inflamm Bowel Dis 2016 Apr;22(4):763-73

*Centre de Recherche sur l'inflammation, Université Paris-Diderot Sorbonne Paris-Cité, Paris, France; †INSERM, UMR 1149, Paris, France; ‡Labex Inflamex, Paris, France; §INRA, MICALIS-UMR1319, Jouy-en-Josas, France; ‖AgroParisTech, MICALISUMR1319, Jouy-en-Josas, France; ¶Assistance Publique Hôpitaux de Paris, Hôpital Robert Debré, Paris, France; **INSERM UMR1163, Laboratory of Intestinal Immunity; Paris, France; ††Université Paris Descartes-Sorbonne Paris Cité and Institut Imagine, Paris, France; and ‡‡INSERM, UMR 1220, Institut de Recherche en Santé Digestive, Université de Toulouse, Toulouse, France.

Background: NOD2 mutations are associated with Crohn's disease (CD). Both CD (in human) and Nod2 deficiency (in mice) are characterized by increased mucosal CD4 T-cells, an altered permeability and a microbial dysbiosis. However, the respective roles of the gut epithelial and immune compartments on the phenotype are not known. Read More

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http://pdfs.journals.lww.com/ibdjournal/2016/04000/Respectiv
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http://content.wkhealth.com/linkback/openurl?sid=WKPTLP:land
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http://dx.doi.org/10.1097/MIB.0000000000000749DOI Listing
April 2016
28 Reads

Disease duration and age influence CARD15 expression in Crohn's disease.

Postepy Hig Med Dosw (Online) 2016 Jan 5;70:10-3. Epub 2016 Jan 5.

Department of Forensic Science, Wroclaw Medical University, Poland.

One of the susceptibility genes in Crohn's disease (CD) is CARD15. Our study examined the relationship between peripheral CARD15 expression and phenotype and duration of CD, treatment methods and inflammatory indices. Sixty patients with CD and 30 healthy volunteers as controls were enrolled in the study. Read More

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http://dx.doi.org/10.5604/17322693.1192187DOI Listing
January 2016
3 Reads

Autoinflammatory granulomatous diseases: from Blau syndrome and early-onset sarcoidosis to NOD2-mediated disease and Crohn's disease.

RMD Open 2015 20;1(1):e000097. Epub 2015 Jul 20.

Rheumatology Unit, Department of Medicine DIMED , University of Padova , Padova , Italy.

The recent identification of genetic mutations leading to dysfunction of inflammatory and apoptotic pathways, has allowed to characterise a group of diseases, recognised as monogenic autoinflammatory syndromes. Among those, Blau syndrome (BS) and early-onset sarcoidosis (EOS) have been identified as familial and sporadic phenotypes of the same non-caseating granulomatous form. Both the diseases are caused by mutations in the CARD15/NOD2 gene, encoding the cytosolic NOD2 protein, one of the key molecules in the regulation of innate immunity. Read More

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http://dx.doi.org/10.1136/rmdopen-2015-000097DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4612691PMC
October 2015
21 Reads

NOD2/CARD15 mutations and the risk of reoperation in patients with Crohns disease.

Rozhl Chir 2015 Jun;94(6):242-6

Introduction: Three NOD2/CARD15 gene variants (3020insC, R702W, G908R) have been identified as genetic risk factors for Crohns disease patients. However the diagnostic and therapeutic relevance for clinical practice remains limited. The aim of this study was to evaluate the association between these variants, the risk of reoperation and disease phenotype. Read More

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June 2015
3 Reads

NOD2/CARD15 gene mutations in North Algerian patients with inflammatory bowel disease.

World J Gastroenterol 2015 Jul;21(25):7786-94

Aziza Boukercha, Hamida Mesbah-Amroun, Amira Bouzidi, Chafia Touil-Boukoffa, Team Cytokines and NO Synthases, Laboratory of Cellular and Molecular Biology, Faculty of Biological Sciences, University of Sciences and Technology Houari Boumediene, Algiers 16111, Algeria.

Aim: To analyse allelic frequency of NOD2 gene variants and to assess their correlation with inflammatory bowel disease (IBD) in Algeria.

Methods: We studied 132 unrelated patients diagnosed with IBD, 86 with Crohn's disease (CD) and 46 with ulcerative colitis (UC). Data was prospectively collected between January 2011 and December 2013. Read More

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http://www.wjgnet.com/1007-9327/full/v21/i25/7786.htm
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http://dx.doi.org/10.3748/wjg.v21.i25.7786DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4491965PMC
July 2015
11 Reads

CARD15 gene overexpression reduces effect of etanercept, infliximab, and adalimumab on cytokine secretion from PMA activated U937 cells.

Eur J Pharmacol 2015 Sep 21;762:394-401. Epub 2015 Jun 21.

Pediatric Infectious Diseases Research Center, Department of Infectious Diseases, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran; Cell and Molecular Biology Department, Pharmaceutical Science Branch, Islamic Azad University, Tehran, Iran.

Crohn's disease (CD), a subcategory of inflammatory bowel disease, is an immune-related disorder characterized by inflammation of the gastrointestinal mucosa, which can take place in any region along the alimentary tract. The most important gene involved in the etiology of CD is NOD2/CARD15 located on chromosome 16. It has been shown that CARD15 is overexpressed in monocytes of CD patients. Read More

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http://dx.doi.org/10.1016/j.ejphar.2015.06.033DOI Listing
September 2015
3 Reads

NOD2/CARD15 mutations in Polish and Bosnian populations with and without Crohn's disease: prevalence and genotype-phenotype analysis.

Bosn J Basic Med Sci 2015 May 25;15(2):67-72. Epub 2015 May 25.

Department of Gastroenterology and Hepatology University Clinical Center Tuzla.

Data on prevalence and phenotypic consequences of nucleotide-binding oligomerisation domain 2/caspase recruitment domains 15 (NOD2/CARD15) variants in Crohn's disease (CD) population in Poland and Bosnia and Herzegovina (B&H) are nonexistent. We aimed to determine the prevalence of NOD2/CARD15 mutations and their association with disease phenotype in Polish and Bosnian patients with CD and in healthy controls. We prospectively recruited 86 CD patients and 83 controls in Poland and 30 CD patients and 30 controls in B&H, 229 in total. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4469939PMC
http://dx.doi.org/10.17305/bjbms.2015.348DOI Listing
May 2015
9 Reads

NOD2/CARD15 gene influences disease behaviour but not IBD susceptibility in a Moroccan population.

Turk J Gastroenterol 2014 Dec;25 Suppl 1:122-8

Laboratory of Medical Genetics, Medical School of Casablanca, Casablanca, Morocco; Center of Doctoral Sciences " in Health Sciences", University Ain Chock Hassan ii, Casablanca, Morocco.

Background/aims: IBD (Crohn's disease and Ulcerative Colitis) is chronic and multifactorial disease of the gastrointestinal tract. Till now, his pathogenesis remains unclear. It involves innate immunity, environmental component and genetic predisposition. Read More

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http://dx.doi.org/10.5152/tjg.2014.3870DOI Listing
December 2014
3 Reads

Claudin-2 as a mediator of leaky gut barrier during intestinal inflammation.

Tissue Barriers 2015 3;3(1-2):e977176. Epub 2015 Apr 3.

Institute of Clinical Physiology; Department of Gastroenterology; Charité ; Berlin, Germany.

The epithelial tight junction determines the paracellular water and ion movement in the intestine and also prevents uptake of larger molecules, including antigens, in an uncontrolled manner. Claudin-2, one of the 27 mammalian claudins regulating that barrier function, forms a paracellular channel for small cations and water. It is typically expressed in leaky epithelia like proximal nephron and small intestine and provides a major pathway for the paracellular transport of sodium, potassium, and fluid. Read More

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http://dx.doi.org/10.4161/21688370.2014.977176DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4372021PMC
April 2015
5 Reads

Different expression of NOD2 in decidual stromal cells between normal and unexplained recurrent spontaneous abortion women during first trimester gestation.

Int J Clin Exp Pathol 2014 1;7(12):8784-90. Epub 2014 Dec 1.

Department of Obstetrics and Gynecology, Sun Yatsen Memorial Hospital of Sun Yatsen University Guangzhou, China.

The NOD2 gene, encoding intracellular paternal recognition receptor (PRR) also called caspase activation and recruitment domain 15 (CARD15), is mutated in Crohn's disease, an autoimmune-disorder. Unexplained recurrent spontaneous abortion (URSA) involved in complex auto-immune disorder. However, little is known about the expression of NOD2 protein at maternal-fetal interface with URSA patients. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4313978PMC
October 2015
14 Reads

Pseudomonas fluorescens alters the intestinal barrier function by modulating IL-1β expression through hematopoietic NOD2 signaling.

Inflamm Bowel Dis 2015 Mar;21(3):543-55

*Université Paris-Diderot, Paris, France; †INSERM UMR1149, Paris, France; ‡Labex inflamex, Sorbonne Paris-Cité, Paris, France; §INSERM UMR1163, Laboratory of Intestinal Immunity, Paris, France; ‖Université Paris Descartes-Sorbonne Paris Cité and Institut Imagine, Paris, France; ¶LMSM EA 4312, Université de Rouen, Evreux, France; **Assistance Publique Hôpitaux de Paris, Hôpital Robert Debré, Paris, France; and ††INSERM UMR 1043, Centre de Physiopathologie de Toulouse, Université de Toulouse, Toulouse, France.

Background: Ileal Crohn's disease is related to NOD2 mutations and to a gut barrier dysfunction. Pseudomonas fluorescens has also been associated with ileal Crohn's disease. The aim of this study was to determine the impact of P. Read More

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http://pdfs.journals.lww.com/ibdjournal/2015/03000/Pseudomon
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http://dx.doi.org/10.1097/MIB.0000000000000291DOI Listing
March 2015
10 Reads

Crohn's disease: a role of gut microbiota and Nod2 gene polymorphisms in disease pathogenesis.

Acta Medica (Hradec Kralove) 2014 ;57(3):89-96

Department of Immunology and Gnotobiology, Institute of Microbiology, Academy of Sciences of the Czech Republic, Doly 183, 549 22 Nový Hrádek, Czech Republic.

Crohn's disease is a chronic immune-mediated intestinal inflammation targeted against a yet incompletely defined subset of commensal gut microbiota and occurs on the background of a genetic predisposition under the influence of environmental factors. Genome-wide association studies have identified about 70 genetic risk loci associated with Crohn's disease. The greatest risk for Crohn's disease represent polymorphisms affecting the CARD15 gene encoding nucleotide-binding oligomerization domain 2 (NOD2) which is an intracellular sensor for muramyl dipeptide, a peptidoglycan constituent of bacterial cell wall. Read More

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http://dx.doi.org/10.14712/18059694.2014.46DOI Listing
June 2015
5 Reads

NOD2 stimulation by Staphylococcus aureus-derived peptidoglycan is boosted by Toll-like receptor 2 costimulation with lipoproteins in dendritic cells.

Infect Immun 2014 Nov 25;82(11):4681-8. Epub 2014 Aug 25.

Institute of Medical Microbiology and Hygiene, University of Tübingen, Tübingen, Germany Deutsches Zentrum für Infektionsforschung (DZIF), Partner Side Tübingen, Tübingen, Germany.

Mutations in the nucleotide-binding oligomerization domain-containing protein 2 (NOD2) play an important role in the pathogenesis of Crohn's disease. NOD2 is an intracellular pattern recognition receptor (PRR) that senses bacterial peptidoglycan (PGN) structures, e.g. Read More

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http://dx.doi.org/10.1128/IAI.02043-14DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4249339PMC
November 2014
11 Reads

Peptidoglycan recognition protein 3 and Nod2 synergistically protect mice from dextran sodium sulfate-induced colitis.

J Immunol 2014 Sep 11;193(6):3055-69. Epub 2014 Aug 11.

Indiana University School of Medicine-Northwest, Gary, IN 46408; and

Aberrant immune response and changes in the gut microflora are the main causes of inflammatory bowel disease (IBD). Peptidoglycan recognition proteins (Pglyrp1, Pglyrp2, Pglyrp3, and Pglyrp4) are bactericidal innate immunity proteins that maintain normal gut microbiome, protect against experimental colitis, and are associated with IBD in humans. Nucleotide-binding oligomerization domain 2 (Nod2) is an intracellular bacterial sensor and may be required for maintaining normal gut microbiome. Read More

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http://dx.doi.org/10.4049/jimmunol.1301548DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4157132PMC
September 2014
58 Reads

Bacterial sensor Nod2 prevents inflammation of the small intestine by restricting the expansion of the commensal Bacteroides vulgatus.

Immunity 2014 Aug 31;41(2):311-24. Epub 2014 Jul 31.

Kimmel Center for Biology and Medicine at the Skirball Institute, New York University School of Medicine, New York, NY 10016, USA; Department of Microbiology, New York University School of Medicine, New York, NY 10016, USA. Electronic address:

Unlabelled: Nod2 has been extensively characterized as a bacterial sensor that induces an antimicrobial and inflammatory gene expression program. Therefore, it is unclear why Nod2 mutations that disrupt bacterial recognition are paradoxically among the highest risk factors for Crohn's disease, which involves an exaggerated immune response directed at intestinal bacteria. Here, we identified several abnormalities in the small-intestinal epithelium of Nod2(-/-) mice including inflammatory gene expression and goblet cell dysfunction, which were associated with excess interferon-γ production by intraepithelial lymphocytes and Myd88 activity. Read More

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http://dx.doi.org/10.1016/j.immuni.2014.06.015DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4238935PMC
August 2014
36 Reads

Activation of pattern recognition receptors up-regulates metallothioneins, thereby increasing intracellular accumulation of zinc, autophagy, and bacterial clearance by macrophages.

Gastroenterology 2014 Oct 21;147(4):835-46. Epub 2014 Jun 21.

Department of Internal Medicine, Yale University, New Haven, Connecticut. Electronic address:

Background & Aims: Continuous stimulation of pattern recognition receptors (PRRs), including nucleotide-binding oligomerization domain-2 (NOD2) (variants in NOD2 have been associated with Crohn's disease), alters the phenotype of myeloid-derived cells, reducing production of inflammatory cytokines and increasing microbe clearance. We investigated the mechanisms by which microbial clearance increases in macrophages under these conditions.

Methods: Monocytes were purified from human peripheral blood mononuclear cells and differentiated to monocyte-derived macrophages (MDMs). Read More

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http://dx.doi.org/10.1053/j.gastro.2014.06.024DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4170054PMC
October 2014
5 Reads

Mechanisms that mediate the development of fibrosis in patients with Crohn's disease.

Inflamm Bowel Dis 2014 Jul;20(7):1250-8

*Department of Medicine, †Department of Physiology and Biophysics, and ‡VCU Program for Enteric Neuromuscular Sciences, Medical College of Virginia Campus, Virginia Commonwealth University, Richmond, Virginia.

Crohn's disease is complicated by the development of fibrosis and stricture in approximately 30% to 50% of patients over time. The pathogenesis of fibrostenotic disease is multifactorial involving the activation of mesenchymal cells by cytokines, growth factors, and other mediators released by immune cells, epithelial cells, and mesenchymal cells. Transforming growth factor β, a key activator of mesenchymal cells, is central to the process of fibrosis and regulates numerous genes involved in the disordered wound healing including collagens, and other extracellular matrix proteins, connective tissue growth factor, and insulin-like growth factors. Read More

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http://dx.doi.org/10.1097/MIB.0000000000000043DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4057349PMC
July 2014
5 Reads

Prediction of Crohn's disease aggression through NOD2/CARD15 gene sequencing in an Australian cohort.

World J Gastroenterol 2014 May;20(17):5008-16

Maneesha Bhullar, Finlay Macrae, Gregor Brown, Department of Colorectal Medicine and Genetics, 3 Centre, The Royal Melbourne Hospital, Parkville 3052, Australia.

Aim: To investigate the association between mutations in oligomerisation domain 2/caspase recruitment domains 15 (NOD2/CARD15) and the natural history of Crohn's disease (CD) to identify patients who would benefit from early aggressive medical intervention.

Methods: We recruited thirty consecutive unrelated CD patients with a history of ileo-caecal or small bowel resection during the period 1980-2000; Fifteen patients of these had post-operative relapse that required further surgery and fifteen did not. Full sequencing of the NOD2/CARD15 gene using dHPLC for exons 3, 5, 7, 10 and 12 and direct sequencing for exons 2, 4, 6, 8, 9 and 11 was conducted. Read More

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http://dx.doi.org/10.3748/wjg.v20.i17.5008DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4009534PMC
May 2014
3 Reads

Association between NOD2/CARD15 gene polymorphisms and Crohn's disease in Chinese Zhuang patients.

World J Gastroenterol 2014 Apr;20(16):4737-44

Wei-Yan Long, Lan Chen, Cui-Liang Zhang, Rong-Mao Nong, Mei-Jiao Lin, Xiao-Ping Lv, Department of Gastroenterology, the First Affiliated Hospital of Guangxi Medical University, Nanning 530021, Guangxi Zhuang Autonomous Region, China.

Aim: To assess the relationship between the P268S, JW1 and N852S polymorphisms and Crohn's disease (CD) susceptibility in Zhuang patients in Guangxi, China.

Methods: Intestinal tissues from 102 Zhuang [48 CD and 54 ulcerative colitis (UC)] and 100 Han (50 CD and 50 UC) unrelated patients with inflammatory bowel disease and 72 Zhuang and 78 Han unrelated healthy individuals were collected in the Guangxi Zhuang Autonomous Region from January 2009 to March 2013. Genomic DNA was extracted using the phenol chloroform method. Read More

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http://dx.doi.org/10.3748/wjg.v20.i16.4737DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4000511PMC
April 2014
6 Reads

3020insC NOD2/CARD15 polymorphism associated with treatment of colorectal cancer.

Med Oncol 2014 May 10;31(5):954. Epub 2014 Apr 10.

Laboratory of Human Genetics Immunology and Pathology, Faculty of Sciences Tunis El Manar, University of Tunis EL Manar, 2092, Tunis, Tunisia,

Chronic inflammation is closely linked to cancer. The risk of damage by colorectal cancer (CRC) may increase due to autoimmune disease and cryptogenic inflammation. Therefore, genetic factors implicated in the chronic irritation in inflammatory bowel disease such as NOD2/CARD15 may predispose to CRC. Read More

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http://link.springer.com/content/pdf/10.1007/s12032-014-0954
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http://link.springer.com/10.1007/s12032-014-0954-z
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http://dx.doi.org/10.1007/s12032-014-0954-zDOI Listing
May 2014
12 Reads
3 Citations
2.060 Impact Factor

NOD2/CARD15 variants in Malaysian patients with sporadic colorectal cancer.

Genet Mol Res 2014 Mar 19;13(3):7079-85. Epub 2014 Mar 19.

Department of Biomedical Science, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia

Colorectal cancer (CRC) is one of the most common types of cancer in both developed and developing countries. This disease is triggered by and progresses via the sequential accumulation of multiple genetic alterations. In addition, the interaction between low-penetrance genes and environmental factors can also increase the risk of developing CRC. Read More

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http://dx.doi.org/10.4238/2014.March.19.3DOI Listing
March 2014
3 Reads

NOD2/CARD15 and IL23R genetic variability in 204 Algerian Crohn's disease.

Clin Res Hepatol Gastroenterol 2014 Sep 25;38(4):499-504. Epub 2014 Mar 25.

Immunology and Histocompatibility Department, CIB-HOB, AP-HP, IUH and INSERM UMRS940, Saint-Louis Hospital, Paris, France.

NOD2/CARD15 and IL23R gene variants play an important role in the susceptibility to Crohn's disease (CD). Studies of genotype-phenotype relationship suggest that these variants are associated with the development of the disease and specific phenotype. Preliminary reports analyzing the association between these variants have never been made on Algerian CD's. Read More

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http://dx.doi.org/10.1016/j.clinre.2014.02.003DOI Listing
September 2014
4 Reads
6 Citations
1.983 Impact Factor

NOD2 downregulates colonic inflammation by IRF4-mediated inhibition of K63-linked polyubiquitination of RICK and TRAF6.

Mucosal Immunol 2014 Nov 26;7(6):1312-25. Epub 2014 Mar 26.

Mucosal Immunity Section, Laboratory of Host Defenses, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA.

It is well established that polymorphisms of the caspase activation and recruitment domain 15 (CARD15) gene, a major risk factor in Crohn's disease (CD), lead to loss of nucleotide-binding oligomerization domain 2 (NOD2) function. However, a molecular explanation of how such loss of function leads to increased susceptibility to CD has remained unclear. In a previous study exploring this question, we reported that activation of NOD2 in human dendritic cells by its ligand, muramyl dipeptide (MDP), negatively regulates Toll-like receptor (TLR)-mediated inflammatory responses. Read More

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http://dx.doi.org/10.1038/mi.2014.19DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4177019PMC
November 2014
3 Reads

Autophagy genes variants and paediatric Crohn's disease phenotype: a single-centre experience.

Dig Liver Dis 2014 Jun 19;46(6):512-7. Epub 2014 Mar 19.

Department of Translational Medical Sciences, Section of Pediatrics, University of Naples "Federico II", Italy.

Background And Aims: Little evidence demonstrating the correlation between several single nucleotide polymorphisms and a specific phenotype of Crohn's disease has been reported in children. We investigated the relationship between autophagy genes variants and clinical features in our children with Crohn's disease.

Methods: Genotyping for ATG16L1, NOD2/CARD15, and IRGM1 was performed in 80 consecutive patients with Crohn's disease (median age: 11 years; range: 0. Read More

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http://dx.doi.org/10.1016/j.dld.2014.02.016DOI Listing
June 2014
12 Reads

Functional defects in NOD2 signaling in experimental and human Crohn disease.

Gut Microbes 2014 May-Jun;5(3):340-4. Epub 2014 Mar 5.

Department of Medicine; Case Western Reserve University; Cleveland, OH USA; Digestive Health Research Center; Case Western Reserve University; Cleveland, OH USA.

Increasing evidence suggests that a deficit in innate immunity may play a causative role in the pathogenesis of inflammatory bowel disease. The most compelling support for this hypothesis comes from the genetic association of Crohn disease (CD) with carriage of polymorphisms within the NOD2 gene, which represent the most frequent genetic defect in CD. Our findings suggest that SAMP1/YitFc mice, which develop CD-like ileitis in the absence of NOD2 genetic mutations, fail to respond to MDP administration by displaying decreased innate cytokine production and impaired bacterial clearance before the onset of disease. Read More

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http://dx.doi.org/10.4161/gmic.28404DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4153771PMC
May 2015
7 Reads

NOD2 regulates CXCR3-dependent CD8+ T cell accumulation in intestinal tissues with acute injury.

J Immunol 2014 Apr 3;192(7):3409-18. Epub 2014 Mar 3.

Department of Medicine, Yale University School of Medicine, New Haven, CT 06520;

Polymorphisms in NOD2 confer risk for Crohn's disease, characterized by intestinal inflammation. How NOD2 regulates both inflammatory and regulatory intestinal T cells, which are critical to intestinal immune homeostasis, is not well understood. Anti-CD3 mAb administration is used as therapy in human autoimmune diseases, as well as a model of transient intestinal injury. Read More

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http://dx.doi.org/10.4049/jimmunol.1302436DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4064676PMC
April 2014
5 Reads

Detection of Mycobacterium avium subspecies paratuberculosis in patients with Crohn's disease is unrelated to the presence of single nucleotide polymorphisms rs2241880 (ATG16L1) and rs10045431 (IL12B).

Med Microbiol Immunol 2014 Jun 13;203(3):195-205. Epub 2014 Feb 13.

Department of Microbiology, University College Cork, Cork, Ireland.

Mycobacterium avium subspecies paratuberculosis (MAP) has been controversially linked with Crohn's disease (CD). Detection of MAP in CD has been highly variable, and one explanation might be the genetic heterogeneity of this syndrome. Many of the single nucleotide polymorphisms (SNPs) linked with CD are contained within genes that are associated with bacterial handling in general, and some are specifically implicated in susceptibility to mycobacterial disease. Read More

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http://dx.doi.org/10.1007/s00430-014-0332-7DOI Listing
June 2014
7 Reads

NOD2/CARD15 single nucleotide polymorphism 13 (3020insC) is associated with risk of sepsis and single nucleotide polymorphism 8 (2104C>T) with herpes viruses reactivation in patients after allogeneic hematopoietic stem cell transplantation.

Biol Blood Marrow Transplant 2014 Mar 15;20(3):409-14. Epub 2013 Dec 15.

Lower Silesian Center for Cellular Transplantation with National Bone Marrow Donor Registry, Wroclaw, Poland.

Three NOD2 polymorphisms (single nucleotide polymorphism [SNP]8 [2104C>T, Arg702Trp], SNP12 [2722G>C, Gly908Arg], and SNP13 [3020insC, Leu1007 fsins C]), identified as disease-associated variants in Crohn's disease, have recently been suggested as gene markers of the outcome of hematopoietic stem cell transplantation (HSCT). In the present multicenter study of 464 donor-recipient pairs, we focused on the effect of NOD2 mutation(s) on the risk of infections and acute graft-versus-host disease (aGVHD). The presence of SNP13 in recipients, donors, or both was more frequently seen in patients having sepsis than in those lacking sepsis (9 of 48 versus 33 of 386, P = . Read More

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http://dx.doi.org/10.1016/j.bbmt.2013.12.558DOI Listing
March 2014
37 Reads
8 Citations
3.404 Impact Factor

[Possibilities of genetic diagnostics of intestine tumour and inflammatory diseases in Slovakia].

Vnitr Lek 2013 Nov;59(11):977-80

In recent years, gastroenterologists focused their interest on finding the genetic background of inflammatory bowel disease and colon cancer. NOD2/ CARD15 gene is still the most investigated gene of all known genes and its mutations can explain approximately 20% of genetic predisposition to Crohns disease. From later identified genes that play an important role in the etiology of Crohns disease, the IL23R and ATG16L1 genes have a perspective place. Read More

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November 2013
3 Reads

The protein ATG16L1 suppresses inflammatory cytokines induced by the intracellular sensors Nod1 and Nod2 in an autophagy-independent manner.

Immunity 2013 Nov;39(5):858-73

Department of Immunology, University of Toronto, Toronto M5S1A8, Canada.

The peptidoglycan sensor Nod2 and the autophagy protein ATG16L1 have been linked to Crohn's disease (CD). Although Nod2 and the related sensor, Nod1, direct ATG16L1 to initiate anti-bacterial autophagy, whether ATG16L1 affects Nod-driven inflammation has not been examined. Here, we uncover an unanticipated autophagy-independent role for ATG16L1 in negatively regulating Nod-driven inflammatory responses. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S10747613130047
Publisher Site
http://dx.doi.org/10.1016/j.immuni.2013.10.013DOI Listing
November 2013
12 Reads