Journal of neuroimmunology · 2025
Association of interleukins 17A and 22 levels and their common genetic polymorphisms in Guillain Barré syndrome.
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Iqbal Afifa, Mubarak Bushra, Amar Ali, Mukhtar Shahid, Khaliq Saba, Tahir Romeeza
Аннотация
BACKGROUND: Guillain-Barré syndrome (GBS) is an autoimmune and multifactorial disorder. Its immunopathogenesis involves activation of the aberrant Th17 pathway. Serum levels of Th17-associated cytokines (IL-17A and IL-22) and their genetic variants were compared between GBS patients and healthy controls.
SUBJECTS AND METHODS: Forty clinically diagnosed acute-phase patients with GBS and 40 healthy controls of Pakistani origin were included. Serum IL-17A and IL-22 levels were determined by ELISA. IL-22 and IL-17A gene variants were genotyped using PCR-RFLP and confirmed by Sanger sequencing. Functional significance analyses of both SNPs were performed using two modern databases: RegulomeDB version 2.2, and GTEx version 10. Data was analyzed using SPSS version 24, SNPatats, Vassarstats odds ratio calculator, and GraphPad Prism software.
RESULTS: Mean ± SD age of GBS patients was more (42.03 ± 11.2 years) than control group (37.5 ± 12.1 years) (p-value = 0.09). Male to female ratio was 2.3:1. Serum levels of IL-17A and IL-22 were higher in GBS patients than in healthy controls (p < 0.0001). For IL-22 rs2227485, the presence of variant alleles in homozygous (A/A) and heterozygous (G/A) alleles was strongly associated with susceptibility to GBS (ORs = 13.17 and 5.73, respectively, p = 0.0001). IL-17A rs3748067 SNP did not show a statistically significant association with GBS. The presence of the variant allele of the IL-22 SNP was associated with increased levels of cytokines in a dose-dependent manner (p < 0.0001).
CONCLUSION: IL-17A and IL-22 play important roles in the pathogenesis of GBS. Serum IL-17 and IL-22 cytokines, along with their genetic variants, are aberrant in GBS patients.
SUBJECTS AND METHODS: Forty clinically diagnosed acute-phase patients with GBS and 40 healthy controls of Pakistani origin were included. Serum IL-17A and IL-22 levels were determined by ELISA. IL-22 and IL-17A gene variants were genotyped using PCR-RFLP and confirmed by Sanger sequencing. Functional significance analyses of both SNPs were performed using two modern databases: RegulomeDB version 2.2, and GTEx version 10. Data was analyzed using SPSS version 24, SNPatats, Vassarstats odds ratio calculator, and GraphPad Prism software.
RESULTS: Mean ± SD age of GBS patients was more (42.03 ± 11.2 years) than control group (37.5 ± 12.1 years) (p-value = 0.09). Male to female ratio was 2.3:1. Serum levels of IL-17A and IL-22 were higher in GBS patients than in healthy controls (p < 0.0001). For IL-22 rs2227485, the presence of variant alleles in homozygous (A/A) and heterozygous (G/A) alleles was strongly associated with susceptibility to GBS (ORs = 13.17 and 5.73, respectively, p = 0.0001). IL-17A rs3748067 SNP did not show a statistically significant association with GBS. The presence of the variant allele of the IL-22 SNP was associated with increased levels of cytokines in a dose-dependent manner (p < 0.0001).
CONCLUSION: IL-17A and IL-22 play important roles in the pathogenesis of GBS. Serum IL-17 and IL-22 cytokines, along with their genetic variants, are aberrant in GBS patients.