Guillain-Barre syndrome outbreak in Peru: Association with polymorphisms in IL-17, ICAM1, and CD1.
Aged
Antigens, CD1
/ genetics
Body Mass Index
Case-Control Studies
Female
Genetic Predisposition to Disease
Genotype
Guillain-Barre Syndrome
/ genetics
Humans
Intercellular Adhesion Molecule-1
/ genetics
Interleukin-17
/ genetics
Male
Middle Aged
Peru
Polymorphism, Single Nucleotide
Regression Analysis
Risk Factors
CD1
ICAM1
IL-17
Guillain-Barre syndrome
genetic polymorphism
Journal
Molecular genetics & genomic medicine
ISSN: 2324-9269
Titre abrégé: Mol Genet Genomic Med
Pays: United States
ID NLM: 101603758
Informations de publication
Date de publication:
10 2019
10 2019
Historique:
received:
20
03
2019
accepted:
08
08
2019
pubmed:
30
8
2019
medline:
23
6
2020
entrez:
30
8
2019
Statut:
ppublish
Résumé
Guillain-Barre Syndrome (GBS) is considered a complex disorder with significant environmental effect and genetic susceptibility. Genetic polymorphisms in CD1E, CD1A, IL-17, and/or ICAM1 had been proposed as susceptibility genetic variants for GBS mainly in Caucasian population. This study explores the association between selected polymorphisms in these genes and GBS susceptibility in confirmed GBS cases reported in mestizo population from northern Peru during the most recent GBS outbreak of May 2018. A total of nine nonrelated cases and 11 controls were sequenced for the polymorphic regions of CD1A, CD1E, IL-17, and ICAM1. We found a significant protective association between heterozygous GA genotype in ICAM1 (241Gly/Arg) and GBS (p < .047). IL-17 was monomorphic in both controls and patients. No significant differences were found in the frequency of SNPs in CD1A and CD1E between the group with GBS patients and healthy controls. ICAM1 polymorphisms might be considered as potential genetic markers of GBS susceptibility. Further studies with larger sample size will be required to validate these findings.
Sections du résumé
BACKGROUND
Guillain-Barre Syndrome (GBS) is considered a complex disorder with significant environmental effect and genetic susceptibility. Genetic polymorphisms in CD1E, CD1A, IL-17, and/or ICAM1 had been proposed as susceptibility genetic variants for GBS mainly in Caucasian population. This study explores the association between selected polymorphisms in these genes and GBS susceptibility in confirmed GBS cases reported in mestizo population from northern Peru during the most recent GBS outbreak of May 2018.
METHODS
A total of nine nonrelated cases and 11 controls were sequenced for the polymorphic regions of CD1A, CD1E, IL-17, and ICAM1.
RESULTS
We found a significant protective association between heterozygous GA genotype in ICAM1 (241Gly/Arg) and GBS (p < .047). IL-17 was monomorphic in both controls and patients. No significant differences were found in the frequency of SNPs in CD1A and CD1E between the group with GBS patients and healthy controls.
CONCLUSION
ICAM1 polymorphisms might be considered as potential genetic markers of GBS susceptibility. Further studies with larger sample size will be required to validate these findings.
Identifiants
pubmed: 31464097
doi: 10.1002/mgg3.960
pmc: PMC6785440
doi:
Substances chimiques
Antigens, CD1
0
ICAM1 protein, human
0
Interleukin-17
0
Intercellular Adhesion Molecule-1
126547-89-5
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
e00960Informations de copyright
© 2019 INBIOMEDIC. Molecular Genetics & Genomic Medicine published by Wiley Periodicals, Inc.
Références
Immunity. 2005 Jun;22(6):763-72
pubmed: 15963790
Cell Mol Immunol. 2018 Jun;15(6):547-562
pubmed: 29375121
Pediatr Rev. 2012 Apr;33(4):164-70; quiz 170-1
pubmed: 22474113
Autoimmun Rev. 2017 Jan;16(1):96-101
pubmed: 27666816
Brain. 2000 Jun;123 ( Pt 6):1092-101
pubmed: 10825349
Inflamm Bowel Dis. 2008 Apr;14(4):437-45
pubmed: 18088064
Mol Psychiatry. 2003 Mar;8(3):257-8
pubmed: 12660796
J Allergy Clin Immunol. 2006 Apr;117(4):795-801
pubmed: 16630936
Mayo Clin Proc. 2017 Mar;92(3):467-479
pubmed: 28259232
Scand J Immunol. 2010 Aug;72(2):134-41
pubmed: 20618772
Ann Neurol. 1998 Jul;44(1):70-5
pubmed: 9667594
Invest Ophthalmol Vis Sci. 2010 Sep;51(9):4447-50
pubmed: 20445114
J Clin Immunol. 2008 Jan;28(1):44-9
pubmed: 17828618
Lancet. 2005 Nov 5;366(9497):1653-66
pubmed: 16271648
Iran J Public Health. 2015 May;44(5):615-24
pubmed: 26284202
Tissue Antigens. 2000 Aug;56(2):159-61
pubmed: 11019917
Mol Genet Genomic Med. 2019 Oct;7(10):e00960
pubmed: 31464097
Rheumatol Int. 2008 Dec;29(2):173-8
pubmed: 18769923
Rev Peru Med Exp Salud Publica. 2010 Jun;27(2):292-5
pubmed: 21072484
Annu Rev Immunol. 1999;17:297-329
pubmed: 10358761
Cytokine. 2008 Feb;41(2):92-104
pubmed: 18178098
N Engl J Med. 1992 Apr 23;326(17):1130-6
pubmed: 1552914
Stroke. 2010 May;41(5):1038-40
pubmed: 20360547
Tissue Antigens. 1999 Aug;54(2):122-7
pubmed: 10488738
Trends Immunol. 2011 May;32(5):232-9
pubmed: 21493143
Q J Med. 1990 Dec;77(284):1297-304
pubmed: 2290923
J Neurol Sci. 1987 Nov;81(2-3):239-45
pubmed: 3694230
J Neuroimmunol. 2006 Aug;177(1-2):112-8
pubmed: 16820217
Neurology. 2011 Mar 15;76(11):968-75
pubmed: 21403108
Ital J Neurol Sci. 1994 Sep;15(6):267-71
pubmed: 7531188
Int J Neurosci. 2017 Aug;127(8):680-687
pubmed: 27595159
J Neuroimmunol. 2007 May;186(1-2):201-2
pubmed: 17434603