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Comparing mannose binding lectin genetic diversity in intracellular and extracellular pathogens
Abstract
One of the important immunological factors in diseases is mannose binding lectin (MBL). The aim of present study is to determine the distribution of the alleles of mannose-binding lectin gene codon 52,
54, 57 and promoter variants H/L, X/Y, P and Q in confirmed VL patients as an intracellular pathogen while compares with extracellular pathogens (in renal infection) and seek correlation between these
variants and intracellular and extracellular infections. Fifty eight confirmed VL patients’ blood samples were compared with fifty eight blood samples of patients received renal in results of renal infections.
MBL genotypes were investigated by polymerase chain reaction and restriction fragment length polymorphism. Frequency of defective allele B in extracellular pathogens was more than intracellular pathogens (P = 0.0001), and in contrary prevalence of wild type allele A in intracellular pathogens was more than extracellular pathogens (P = 0.0001), and in other alleles and variants there was not any significant difference. In conclusion, there was more prevalence of alleles with low mannose binding lectin serum level in extrallelular pathogens which can be consider as a risk factor for these infections. In other hand prevalence of high concentration alleles in intracellular pathogens indicate the role of mannose binding lectin level for susceptibility to intracellular pathogens.
54, 57 and promoter variants H/L, X/Y, P and Q in confirmed VL patients as an intracellular pathogen while compares with extracellular pathogens (in renal infection) and seek correlation between these
variants and intracellular and extracellular infections. Fifty eight confirmed VL patients’ blood samples were compared with fifty eight blood samples of patients received renal in results of renal infections.
MBL genotypes were investigated by polymerase chain reaction and restriction fragment length polymorphism. Frequency of defective allele B in extracellular pathogens was more than intracellular pathogens (P = 0.0001), and in contrary prevalence of wild type allele A in intracellular pathogens was more than extracellular pathogens (P = 0.0001), and in other alleles and variants there was not any significant difference. In conclusion, there was more prevalence of alleles with low mannose binding lectin serum level in extrallelular pathogens which can be consider as a risk factor for these infections. In other hand prevalence of high concentration alleles in intracellular pathogens indicate the role of mannose binding lectin level for susceptibility to intracellular pathogens.