Abstract
Microorganisms adhere to uroepitelium and trigger adaptive immune response with synthesis of chemokine’s and cytokines. Chemokine and chemokine receptors lead to recruitment of inflammatory cells results in inflammatory response: healing or scaring. FcR initiates effector functions: degranulation, cytokine, superoxide production, and arrangement of antibody synthesis, antibody dependent cellular cytotoxicity, and phagocytosis. Aim was to determine FcγR polymorphism role in urinary tract infection (UTI). 131 UTI and 151 healthy subjects without any urinary tract abnormality were participated. Polymorphisms were determined by amplification refractory mutation system PCR. FcγRIIa R/R genotype and FcγRIIa R allele are found significantly higher in study group than control. FcγRIIIa genotype distribution and allele frequency is not significantly different between UTI and control group. FcγRIIIb-NA2/NA2 genotype and NA2 allele are found statistically higher when compared to control FcgRIIa-131-R allele is found to be related; lower UTI (p=0.015), gram negative bacterial infection risk (p=0.012) FcgRIIIb-NA2 allele is found to be related; upper UTI (p=0.001) gram negative bacterial infection (p=0.001), renal scar development risk (p=0.001). FcγRIIa-R131R and FcγRIIIb-NA2/NA2 gene polymorphisms may increase risk and susceptibility to UTI in children.
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