Mannose Binding Lectin Serum Level and Gene Polymorphism in Patients with SLE and Its Relation to the Development of Lupus Nephritis

Kamal Okasha; Abeer Shahba; Nashwa Noor-eldeen; Azza Hassan; Hanan El-saadany; Amal El-Bendary

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Mannose Binding Lectin Serum Level and Gene Polymorphism in Patients with SLE and Its Relation to the Development of Lupus Nephritis

Author(s):

Kamal Okasha^1,*,

Abeer Shahba²,

Nashwa M. Noor-eldeen²,

Azza M. Hassan²,

Hanan El-saadany²,

Amal El-Bendary²

1Department of Internal Medicine/Nephrology Division,Faculty of medicine, Tanta University, okasha70@yahoo.com, Egypt

2Department of Internal Medicine/Nephrology Division,Faculty of medicine, Tanta University, Egypt

Nephro-Urology Monthly:Vol. 2, issue 3; 401-413

Article type:Research Article

Received:Oct 02, 2009

Accepted:Nov 04, 2009

How to Cite:Kamal OkashaAbeer ShahbaNashwa M. Noor-eldeenAzza M. HassanHanan El-saadanyAmal El-Bendaryet al.Mannose Binding Lectin Serum Level and Gene Polymorphism in Patients with SLE and Its Relation to the Development of Lupus Nephritis.Nephro-Urol Mon.2(3):401-413.

Abstract

Background and Aims: Systemic lupus erythematosus (SLE) is an autoimmune disease in which the complement system plays a crucial role in its pathogenesis. Mannan-binding lectin (MBL) is a recognition molecule of the lectin pathway of complement activation. The presence of several polymorphisms at the promoter and coding regions of the MBL-2 gene determines alterations at MBL serum concentration. MBL variant alleles that lead to low serum levels and/or functional deficits of MBL are postulated to contribute to the susceptibility of SLE. Moreover, the influence of MBL variation on antibody production and renal involvement in SLE patients remains controversial. Objectives: MBL serum level and genotypes were studied in our SLE Egyptian patients with evaluation of its role in auto antibodies production and lupus nephritis development.

Methods: MBL genotypes and serum level were screened in a case control study included 30 SLE patients as well as 30 healthy controls. MBL polymorphism at exon 1 codons 54 and 57 was detected by PCR using sequence-specific priming (SSP) and serum MBL level was determined by ELISA technique.

Results: There was predominance of AA genotype (80%) in control group. Genotype frequencies of MBL variants in patients with SLE showed significant differences when compared with controls (AA 53.3% vs 80%, P=0.03, OR = 0.29 and AO+OO 46.6% vs 20%, P = 0.03, OR = 3.5, respectively). Serum MBL in our SLE patients (900 ng/ml) was significantly lower than that of the control group (2750 ng/ml, P = 0.00) with positive correlation with low MBL genotypes. SLE patients with mutant alleles were more likely to produce anti dsDNA (92.8% vs 75%, OR = 4.3) and anti-Smith (35.7% vs 18.7%, OR = 2.3). Patients carrying MBL-low genotypes have an increased risk of development of lupus nephritis than those carrying MBL-high genotype (64.7% vs 35.2%, P = 0.02, OR= 2.4).

Conclusion: MBL gene polymorphism associated with low MBL serum levels that were found with significantly increased frequency in our SLE patients may be one of the genetic factors that determine the susceptibility to develop lupus nephritis.

Keywords

Mannose-Binding Lectin (MBL)

Systemic Lupus Erythematosus (SLE)

Lupus Nephritis (LN)

Gene Polymorphism

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