Polymorphism of the Monocyte Chemoattractant Protein 1 Gene in Children with Lupus Nephritis
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- Category: Vol. 78, March 2010
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Polymorphism of the Monocyte Chemoattractant Protein 1 Gene in Children with Lupus Nephritis,HEBA M. SHARAF ELDEEN, SAMAR M. SABRY and EMAN KHLIFA
Abstract
Background: Lupus nephritis is a major contributor to morbidity and mortality in patients with systemic lupus erythematosus (SLE). Biopsy-proven lupus nephritis (LN) occur in around 80% of all cases of childhood-onset SLE. The etiology of SLE remains unknown. However, there is evidence that both genetic and environmental factors play a role in disease development.
Urinary biomarkers are easily obtained and they specifcally represent local renal inflammatory activity. Among the potential urinary biomarkers is Monocyte chemoattractant Protein-1 (MCP-1) which is a chemokine (CC) that is mainly expressed by activated monocytes/macrophages leucocytes and other mediators into sites of inflammation. There is evidence that polymorphisms in the genes of inflammatory mediators may predispose to the development of LN.
Aim of the Work: Our study aimed to examine role of a functional MCP-1 polymorphism in children with SLE and LN and to assess the use of urinary MCP-1 as a marker of disease activity in LN.
Subjects and Methods: This study was conducted on 50 subjects, they included 40 SLE patients (>!4 American college of Rheumatology criteria for SLE), 20 with and 20 without LN) and 10 controls.
DNA were obtained and MCP-1 genomic variants were detected by polymerase chain reaction (PCR) followed by Restriction Enzyme Fragment Length Polymorphism (REFLP).
Urinary MCP-1 levels were measured by Enzyme-Liked Immuno Sorbent Assay (ELISA).
Results: The A/A genotype was more common in control (80%) than in SLE patients (52.5%), where as both A/G and G/G genotype were more frequent in SLE patients than in control (p=0.215 for all). The A/A genotype was observed in only 45% of the patients with LN compared with 60% of those without LN. However, these differences did not reach a statistically significant level (p>0.05).
Urinary levels of MCP-1 were significantly higher in patients with LN (p=0.000) Conclusion: These results may suggest a possible role of genetic polymorphism of MCP-1 in the development of SLE and subsequently LN in children which still need further investigations. Moreover, urinary levels of MCP-1 may be a useful marker for the detection and management of LN.