AI Article Synopsis
- - The study examines the role of interleukin (IL)-17A genetic variations (specifically SNPs) in susceptibility to bacterial meningitis (BM) among Angolan children, involving 241 patients and 265 matched controls.
- - A specific SNP variant, rs4711998, was found to be significantly more common in patients with BM from Haemophilus influenzae, indicating a higher risk of infection.
- - Patients with another SNP variation, rs8193036, showed a reduced risk of severe neurological issues linked to Streptococcus pneumoniae, suggesting that certain genetic factors could influence BM outcomes in this population.
Article Abstract
Interleukin (IL)-17 A plays a crucial role in protecting hosts from invading bacterial pathogens. In this study, we investigated if single nucleotide polymorphisms (SNPs) in IL-17A are associated with susceptibility and outcome of bacterial meningitis (BM) in Angolan children. The study sample comprised 241 confirmed BM patients and 265 controls, which were matched for age and ethnicity. Three IL-17A SNPs - rs2275913 (-197G > A), rs8193036 (-737C > T) and rs4711998 (-877 A > G) - were determined by high-resolution melting analysis (HRMA). The frequency of variant genotype rs4711998 was significantly higher in patients with BM caused by Haemophilus influenzae (odds ratio [OR] 3.5; 95% confidence interval [CI] 1.49-8.23; P = 0.0025) than in controls. Also, patients with BM caused by Gram-negative bacteria and who carried the variant genotype rs2275913 had a lower glucose level (P = 0.0051) in cerebrospinal fluid (CSF). Patients with BM caused by Streptococcus pneumoniae who carried the variant type rs8193036 had a reduced risk for severe neurological sequelae (OR: 0.14; 95% CI: 0.029-0.68; P = 0.0079), blindness (OR: 0.012; 95% CI: 0.012-0.87; P = 0.017) and ataxia (OR: 0.28; 95% CI: 0.091-0.83; P = 0.023). This study suggests an association of IL-17A genetic variations with susceptibility and outcome of bacterial meningitis in Angolan children.
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| http://dx.doi.org/10.1016/j.meegid.2024.105553 | DOI Listing |
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