Study of Mannose-Binding Lectin Gene and Promoter Polymorphism in Kidney Infections

Research Article
Study of Mannose-Binding Lectin Gene and Promoter Polymorphism in Kidney Infections

Mohammad Asgharzadeh, Hossein Samadi Kafil, Mohammad Ebrahim Ebrahimzadeh and Aboulfazl Bohlouli

Research Journal of Microbiology, 2007, 2(7), 596-600.

Abstract

The aim of present study is to determine the distribution of the alleles of mannose-binding lectin gene and promoter variants in infections that cause renal dysfunctions. Fifty eight renal recipients’ samples which lost their kidneys in result of infection have compared with 120 normal controls from Azarbaijan population of Iran. Blood samples were obtained from renal transplant recipients who received renal from March 2004 to July 2005. Mannose-binding lectin genotypes have investigated by polymerase chain reaction and restriction fragment length polymorphism. Allelic and genotypic frequency of the polymorphism at position-550, +4 and at codon 52 and 57 did not show statistical differences between infected patients and controls (p>0.05) but significant frequency of allele B (codon 54) (p = 0.0011) and Ly (p = 0.007), Lx haplotype (p = 0.0002) of promoter was observed in this patients and allele A was more frequent in healthy patients. Present findings provide evidence that presence of different alleles and haplotypes that cause low concentration of mannose-binding lectin in serum is a risk factor for susceptibility to renal infections that cause renal dysfunction.

ASCI-ID: 83-169

Table 1:	Genotype frequency of mannose-binding lectin structural alleles in patients with kidney infection and healthy controls

Mannose-binding lectin variants frequency in patients and controls, *Each Patients has two alleles on its genotype

Table 2:	Frequency of promoter variants and position +4 in patients with kidney infection and Healthy controls

Mannose-binding lectin variants frequency in patients and controls, *Each Patients has two variants on its genotype

Table 3:	Promoter haplotypes frequency in patients with kidney infection and healthy controls

*Mannose-binding lectin variants frequency in patients and controls

MBL gene alleles distribution showed in Table 1. There were more frequency of lower MBL product allele of B in infected patients (p = 0.0011) and more (p = 0.0912) prevalence of healthy allele of A with high production of MBL in serum in normal controls (p = 0.0006). Frequency of promoter variants and position +4 showed in Table 2 and there was not any statistical difference between infected patients with Kidney failure and Normal controls.

In Table 3 we showed frequency of promoter haplotypes between SLE patients with Kidney failure and controls and in HY haplotype, there was not statistical difference, but in Ly with moderate production (p = 0.0074) and LX haplotypes with lower concentration of MBL, frequency in infected patients was higher than normal controls (p = 0.0002).

DISCUSSION

We studied the association between exon 1 and promoter haplotypes and outcome upon infection in Kidney failures, we have shown that genotypes with Low MBL concentration were more frequency among patients had kidney infection than healthy controls and on the contrary genotypes with high MBL serum levels were more frequent among healthy individuals in comparing with infected patients, In structural alleles of MBL, allele B in lower MBL concentration was more frequent in Infected patients (p = 0.0011) and allele A with highest concentration of MBL was more frequent in Healthy controls in comparing with infected patients (p = 0.0912), in promoter haplotypes we had a same situation and Ly haplotype and Lx haplotype with low MBL concentration were more frequent in Infected patients with kidney failures.

MBL have different roles in infections, in intracellular infections deficiency confers protection against these infections. In tuberculosis has been demonstrated that heterozygosity for MBL variant allele (XA/O), which encodes low serum MBL level is associated with protection against clinical turberculosis (Bellamy and Hill, 1998; Soborg et al., 2003) or a new study suggest a protective role for MBL deficiency against development of the most severe and multi bacillary form of leprosy but not the tuberculoid form (Dornelles et al., 2006). Also in intracellular parasite like Leishmania increasing concentration of MBL cause increasing the release of TNF- and interleukin 6 from monocytes contaminated with parasite (Jack et al., 2003). In extracellular infections there is conversion and MBL deficiency may confer a life-long risk of infections (Summerfield et al., 1995). MBL acts as a complement activator to kill gram-negative organisms directly via the membrane-attack complex or to enhance complement-mediated phagocytosis through the increased deposition of opsonic C3 fragments (Jack et al., 2001a) as an extra cellular pathogen. In aspergillosis codon 52 mutation was particularly common that demonstrated MBL low serum level as a risk factor for chronic necrotizing pulmonary aspergillosis (Crosdale et al., 2001).

The most important cause of Kidney failures are extracellular pathogens like Escherichia coli or Proteus species and in our study all species accumulated from patients’ loss their kidneys in result of infections and as results showed defective alleles and haplotypes of MBL were more frequent in these patients.

In conclusion High-expression MBL genotypes can be associate with protection against infections cause to renal failures and defective alleles with low MBL level can be consider as a risk factor for kidney infections.

ACKNOWLEDGMENTS

This study was supported by a grant from Tabriz University of Medical Sciences. The authors wish to thank the renal transplantation section of Imam Khomeini Hospital who participated in the collection of samples. Naghmeh Badroghli provided entire background and information of patients.

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