Genetic polymorphisms of rs9313422 G>C and rs41297579 G>A at the promoter of TIM‐1 gene contribute to the risk of community‐acquired pneumonia in children

Objective To investigate the association of genetic polymorphisms of rs9313422 G>C and rs41297579 G>A at the promoter of TIM‐1 gene with the risk of community‐acquired pneumonia (CAP) in children. Methods A total of 112 children with CAP were included as the case group. Another 120 healthy chi...

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Veröffentlicht in:Journal of clinical laboratory analysis 2020-03, Vol.34 (3), p.e23095-n/a
Hauptverfasser: Liu, Yang, Xu, Hong‐Bo
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Sprache:eng
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Zusammenfassung:Objective To investigate the association of genetic polymorphisms of rs9313422 G>C and rs41297579 G>A at the promoter of TIM‐1 gene with the risk of community‐acquired pneumonia (CAP) in children. Methods A total of 112 children with CAP were included as the case group. Another 120 healthy children were enrolled as the control group. Polymerase chain reaction‐restriction fragment length polymorphism (PCR‐RFLP) was applied for the genotyping of rs9313422 G>C and rs41297579 G>A in the promoter region of TIM‐1. Results rs9313422 G>C was related to the risk of CAP in children under codominant model, dominant model, recessive model, and allele model. Besides, the A allele of rs41297579 G>A could increase the risk of CAP in children. Besides, the haplotype GA (rs9313422‐rs41297579) and GG reduced the risk of children CAP, while haplotype CA had an elevated risk. rs9313422 G>C and rs41297579 G>A polymorphisms were both associated with the severity of CAP in children, and the rs9313422 G>C was also related to the ICU admission rate. In addition, patients carried with the mutant homozygotes of rs9313422 G>C and rs41297579 G>A showed higher levels of white blood cell (WBC), procalcitonin (PCT), and C‐reactive protein (CRP) than the wild type and heterozygous genotypes carriers. Conclusion rs9313422 G>C and rs41297579 G>A polymorphisms in the promoter region of TIM‐1 could increase the risk of CAP in children and showed a relation with inflammatory responses and severity.
ISSN:0887-8013
1098-2825
DOI:10.1002/jcla.23095