Nucleotide oligomerization domain polymorphism confers no risk to Guillain-Barré syndrome.


Journal

Acta neurologica Scandinavica
ISSN: 1600-0404
Titre abrégé: Acta Neurol Scand
Pays: Denmark
ID NLM: 0370336

Informations de publication

Date de publication:
Aug 2022
Historique:
revised: 26 04 2022
received: 19 03 2022
accepted: 06 05 2022
pubmed: 3 6 2022
medline: 15 7 2022
entrez: 2 6 2022
Statut: ppublish

Résumé

Nucleotide oligomerization domain (NOD) proteins are cytoplasmic receptors that play important roles in host innate immune responses to pathogens by recognizing self or non-self-molecules and have been implicated in many autoimmune diseases including Guillain-Barré syndrome (GBS). The current study investigated whether NOD polymorphisms (NOD1-Glu266Lys, rs2075820, and NOD2- [Arg702Trp, rs2066844 and Gly908Arg, rs2066845]) contribute to ligand sensing and thus affect the susceptibility and/or severity of GBS. We determined single nucleotide polymorphisms (SNPs) of NOD gene (NOD1-Glu266Lys and NOD2-[Arg702Trp; Gly908Ar]) in 303 patients with GBS and 303 healthy controls from Bangladesh by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) and Sanger sequencing. Genotypes and allele frequencies were compared by performing chi-squared or Fisher's exact test with Yates' continuity correction. Serology for Campylobacter jejuni and anti-GM1 antibodies were determined by enzyme-linked immunosorbent assay (ELISA) techniques. NOD variants (NOD1-Glu266Lys and NOD2- [Arg702Trp; Gly908Arg]) were not associated with susceptibility and severity of GBS when compared with healthy controls and mild or severe form of disease. Moreover, NOD2 polymorphisms showed wild-type NOD2 C2104 and NOD2 G2722, respectively, with homozygous Arg/Arg genotype of NOD2 (Arg702Trp) polymorphism and homozygous Gly/Gly genotype of NOD2 (Gly908Arg) for all study subjects in Bangladesh. Homogenous distribution of NOD1 genotypes was observed in patients with axonal and demyelinating form of GBS. NOD variants confer no risk to the susceptibility and severity of GBS. Moreover, NOD2 polymorphism is rare or absent in patients with GBS as well as in the healthy individuals of Bangladesh.

Identifiants

pubmed: 35652365
doi: 10.1111/ane.13649
doi:

Substances chimiques

Nucleotides 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

177-185

Subventions

Organisme : icddr,b, Dhaka, Bangladesh

Informations de copyright

© 2022 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.

Références

Winer JB. Guillain Barré syndrome. Mol Pathol. 2001;54(6):381-385.
Islam Z, Gilbert M, Mohammad QD, et al. Guillain-Barré syndrome-related Campylobacter jejuni in Bangladesh: ganglioside mimicry and cross-reactive antibodies. PLoS One. 2012;7(8):e43976. doi:10.1371/journal.pone.0043976
Rose NR. Negative selection, epitope mimicry and autoimmunity. Curr Opin Immunol. 2017;49:51-55. doi:10.1016/J.COI.2017.08.014
Jahan I, Ahammad RU, Khalid MM, et al. Toll-like receptor-4 299Gly allele is associated with Guillain-Barré syndrome in Bangladesh. Ann Clin Transl Neurol. 2019;6(4):708-715. doi:10.1002/acn3.744
Nyati KK, Nyati R. Role of Campylobacter jejuni infection in the pathogenesis of Guillain-Barré syndrome: an update. Biomed Res Int. 2013;2013(85219):13. doi:10.1155/2013/852195
Jacobs BC, Rothbarth PH, van der Meché FGA, et al. The spectrum of antecedent infections in Guillain-Barré syndrome. Neurology. 1998;51(4):1110-1115. doi:10.1212/WNL.51.4.1110
Islam Z, Jacobs BC, van Belkum A, et al. Axonal variant of Guillain-Barre syndrome associated with campylobacter infection in Bangladesh. Neurology. 2010;74(7):581-587. doi:10.1212/WNL.0b013e3181cff735
Olson CK, Ethelberg S, van Pelt W, Tauxe RV. Epidemiology of Campylobacter jejuni infections in industrialized nations. Campylobacter. American Society for Microbiology; 2014:163-189. doi:10.1128/9781555815554.ch9
Nachamkin I. Campylobacter enteritis and the Guillain-Barré syndrome. Curr Infect Dis Rep. 2001;3(2):116-122. doi:10.1007/s11908-996-0033-5
Nyati KK, Nyati R. Role of Campylobacter jejuni infection in the pathogenesis of Guillain-Barré syndrome: an update. Biomed Res Int. 2013;2013:852195. doi:10.1155/2013/852195
Sinha S, Prasad KN, Jain D, Nyati KK, Pradhan S, Agrawal S. Immunoglobulin IgG fc-receptor polymorphisms and HLA class II molecules in Guillain-Barré syndrome. Acta Neurol Scand. 2010;122(1):21-26. doi:10.1111/j.1600-0404.2009.01229.x
Franchi L, Warner N, Viani K, Nuñez G. Function of nod-like receptors in microbial recognition and host defense. Immunol Rev. 2009;227(1):106-128. doi:10.1111/j.1600-065X.2008.00734.x
Takeuchi O, Akira S. Pattern recognition receptors and inflammation. Cell. 2010;140(6):805-820. doi:10.1016/j.cell.2010.01.022
Inohara N, Koseki T, Del Peso L, et al. Nod1, an Apaf-1-like activator of caspase-9 and nuclear factor-κB. J Biol Chem. 1999;274(21):14560-14567. doi:10.1074/jbc.274.21.14560
Ogura Y, Bonen DK, Inohara N, et al. A frameshift mutation in NOD2 associated with susceptibility to Crohn's disease. Nature. 2001;411(6837):603-606. doi:10.1038/35079114
Carneiro LAM, Travassos LH. The interplay between NLRs and autophagy in immunity and inflammation. Front Immunol. 2013;4:361. doi:10.3389/fimmu.2013.00361
Girardin SE, Tournebize R, Mavris M, et al. CARD4/Nod1 mediates NF-kappaB and JNK activation by invasive Shigella flexneri. EMBO Rep. 2001;2(8):736-742. doi:10.1093/embo-reports/kve155
Girardin SE, Boneca IG, Carneiro LAM, et al. Nod1 detects a unique muropeptide from Gram-negative bacterial peptidoglycan. Science. 2003;300(5625):1584-1587. doi:10.1126/science.1084677
Inoue N, Tamura K, Kinouchi Y, et al. Lack of common NOD2 variants in Japanese patients with Crohn's disease. Gastroenterology. 2002;123(1):86-91. doi:10.1053/gast.2002.34155
Kara B, Akkiz H, Doran F, et al. The significance of E266K polymorphism in the NOD1 gene on helicobacter pylori infection: an effective force on pathogenesis? Clin Exp Med. 2009;10:107-112. doi:10.1007/s10238-009-0077-6
Negroni A, Pierdomenico M, Cucchiara S, Stronati L. NOD2 and inflammation: current insights. J Inflamm Res. 2018;11:49-60. doi:10.2147/JIR.S137606
Sansonetti PJ, Arondel J, Huerre M, Harada A, Matsushima K. Interleukin-8 controls bacterial transepithelial translocation at the cost of epithelial destruction in experimental shigellosis. Infect Immun. 1999;67(3):1471-1480. doi:10.1128/iai.67.3.1471-1480.1999
Carneiro L, Magalhaes J, Tattoli I, Philpott D, Travassos L. Nod-like proteins in inflammation and disease. J Pathol. 2008;214(2):136-148. doi:10.1002/path.2271
Orr N, Chanock S. Chapter 1 common genetic variation and human disease. Adv Genet 2008;62:1-32. 10.1016/S0065-2660(08)00601-9
Boguniewicz M, Leung DYM. Atopic dermatitis: a disease of altered skin barrier and immune dysregulation. Immunol Rev. 2011;242(1):233-246. doi:10.1111/j.1600-065X.2011.01027.x
Lu W-G, Zou Y-F, Feng X-L, et al. Association of NOD1 (CARD4) insertion/deletion polymorphism with susceptibility to IBD: a meta-analysis. World J Gastroenterol. 2010;16(34):4348-4356. doi:10.3748/wjg.v16.i34.4348
Tanabe T, Yamaguchi N, Eishi Y, Fujita Y. The roles of NOD like receptors in inflammation are different between Japanese and Caucasian. Inflamm Regen. 2011;31(2):196-201. doi:10.2492/inflammregen.31.196
Kharwar NK, Prasad KN, Paliwal VK, Modi DR. Association of NOD1 and NOD2 polymorphisms with Guillain-Barré syndrome in northern Indian population. J Neurol Sci. 2016;363:57-62. doi:10.1016/j.jns.2016.02.028
Hayat S, Ahmad O, Mahmud I, Howlader MZH, Islam Z. Association of matrix metalloproteinase-9 polymorphism with severity of Guillain-Barré syndrome. J Neurol Sci. 2020;415:116908. doi:10.1016/j.jns.2020.116908
Asbury AK, Cornblath DR. Assessment of current diagnostic criteria for Guillain-Barré syndrome. Ann Neurol. 1990;27(1 S):S21-S24. doi:10.1002/ana.410270707
Kleyweg RP, Van Der Meché FGA, Schmitz PIM. Interobserver agreement in the assessment of muscle strength and functional abilities in Guillain-Barré syndrome. Muscle Nerve. 1991;14(11):1103-1109. doi:10.1002/mus.880141111
Geleijns K, Emonts M, Laman JD, et al. Genetic polymorphisms of macrophage-mediators in Guillain-Barré syndrome. J Neuroimmunol. 2007;190(1-2):127-130. doi:10.1016/j.jneuroim.2007.07.008
Hughes RAC, Newsom-Davis JM, Perkin GD, Pierce JM. Controlled trial of prednisolone in acute polyneuropathy. Lancet. 1978;312(8093):750-753. doi:10.1016/S0140-6736(78)92644-2
Ang CW, Krogfelt K, Herbrink P, et al. Validation of an ELISA for the diagnosis of recent campylobacter infections in Guillain-Barré and reactive arthritis patients. Clin Microbiol Infect. 2007;13(9):915-922. doi:10.1111/J.1469-0691.2007.01765.X
Kuijf ML, van Doorn PA, Tio-Gillen AP, et al. Diagnostic value of anti-GM1 ganglioside serology and validation of the INCAT-ELISA. J Neurol Sci. 2005;239(1):37-44. doi:10.1016/J.JNS.2005.07.009
McGinnis S, Madden TL. BLAST: at the core of a powerful and diverse set of sequence analysis tools. Nucleic Acids Res. 2004;32(suppl_2):W20-W25. doi:10.1093/nar/gkh435
Owczarzy R, Tataurov AV, Wu Y, et al. IDT SciTools: a suite for analysis and design of nucleic acid oligomers. Nucleic Acids Res. 2008;36(suppl_2):W163-W169. doi:10.1093/nar/gkn198
Tamura K, Stecher G, Peterson D, Filipski A, Kumar S. MEGA6: molecular evolutionary genetics analysis version 6.0. Mol Biol Evol. 2013;30(12):2725-2729. doi:10.1093/MOLBEV/MST197
Hadden RDM, Cornblath DR, Hughes RAC, et al. Electrophysiological classification of Guillain-Barre syndrome: clinical associations and outcome. Ann Neurol. 1998;44(5):780-788. doi:10.1002/ana.410440512
Weidinger S, Klopp N, Rummler L, et al. Association of NOD1 polymorphisms with atopic eczema and related phenotypes. J Allergy Clin Immunol. 2005;116(1):177-184. doi:10.1016/j.jaci.2005.02.034
McGovern DPB, Hysi P, Ahmad T, et al. Association between a complex insertion/deletion polymorphism in NOD1 (CARD4) and susceptibility to inflammatory bowel disease. Hum Mol Genet. 2005;14(10):1245-1250. doi:10.1093/hmg/ddi135
Hysi P, Kabesch M, Moffatt MF, et al. NOD1 variation, immunoglobulin E and asthma. Hum Mol Genet. 2005;14(7):935-941. doi:10.1093/hmg/ddi087
Kim JG, Lee SJ, Kagnoff MF. Nod1 is an essential signal transducer in intestinal epithelial cells infected with bacteria that avoid recognition by toll-like receptors. Infect Immun. 2004;72(3):1487-1495. doi:10.1128/IAI.72.3.1487-1495.2004
Arnott IDR, Nimmo ER, Drummond HE, et al. NOD2/CARD15, TLR4 and CD14 mutations in Scottish and Irish Crohn's disease patients: evidence for genetic heterogeneity within Europe? Genes Immun. 2004;5(5):417-425. doi:10.1038/sj.gene.6364111
Cavanaugh J. NOD2: ethnic and geographic differences. World J Gastroenterol. 2006;12(23):3673-3677. doi:10.3748/wjg.v12.i23.3673
Lee GH, Kim CG, Kim JS, Jung HC, Song IS. Frequency analysis of NOD2 gene mutations in Korean patients with Crohn's disease. Korean J Gastroenterol. 2005;45(3):162-168.
Doets AY, Verboon C, van den Berg B, et al. Regional variation of Guillain-Barré syndrome. Brain. 2018;141(10):2866-2877. doi:10.1093/brain/awy232

Auteurs

Shoma Hayat (S)

Laboratory of Gut-Brain Signaling, Laboratory Sciences and Services Division (LSSD), Dhaka, Bangladesh.

Asaduzzaman Asad (A)

Laboratory of Gut-Brain Signaling, Laboratory Sciences and Services Division (LSSD), Dhaka, Bangladesh.

Imran Hasan (I)

Laboratory of Gut-Brain Signaling, Laboratory Sciences and Services Division (LSSD), Dhaka, Bangladesh.

Israt Jahan (I)

Laboratory of Gut-Brain Signaling, Laboratory Sciences and Services Division (LSSD), Dhaka, Bangladesh.

Nowshin Papri (N)

Laboratory of Gut-Brain Signaling, Laboratory Sciences and Services Division (LSSD), Dhaka, Bangladesh.

Zakir Hossain Howlader (ZH)

Department of Biochemistry and Molecular Biology, University of Dhaka, Dhaka, Bangladesh.

Zhahirul Islam (Z)

Laboratory of Gut-Brain Signaling, Laboratory Sciences and Services Division (LSSD), Dhaka, Bangladesh.

Articles similaires

[Redispensing of expensive oral anticancer medicines: a practical application].

Lisanne N van Merendonk, Kübra Akgöl, Bastiaan Nuijen
1.00
Humans Antineoplastic Agents Administration, Oral Drug Costs Counterfeit Drugs

Smoking Cessation and Incident Cardiovascular Disease.

Jun Hwan Cho, Seung Yong Shin, Hoseob Kim et al.
1.00
Humans Male Smoking Cessation Cardiovascular Diseases Female
Humans United States Aged Cross-Sectional Studies Medicare Part C
1.00
Humans Yoga Low Back Pain Female Male

Classifications MeSH