International Journal of
Genetics and Molecular Biology

  • Abbreviation: Int. J. Genet. Mol. Biol.
  • Language: English
  • ISSN: 2006-9863
  • DOI: 10.5897/IJGMB
  • Start Year: 2009
  • Published Articles: 131

Review

Evaluation of the association between ICAM-1 gene polymorphisms and sICAM-1 serum levels in multiple sclerosis (MS) patients in Southeast Iran

Nima Sanadgol1*, Abbas Nikravesh1, Gholamreza Motalleb1, Fariba Roshanzamir1, Toktam Balazade1, Nourollah Ramroodi2 and Hamideh Khajeh3
1Department of Biology, Faculty of Science, Zabol University, Zabol, Iran. 2Department of Neurology, Zahedan University of Medical Science, Zahedan, Iran. 3Agricultural Biotechnology Research Institute (Biocenter), Zabol University, Zabol, Iran
Email: [email protected], [email protected]

  •  Accepted: 23 May 2011
  •  Published: 30 July 2011

Abstract

Multiple sclerosis (MS) is an autoimmune nervous system disorder characterized by leukocytes recruitment into nervous system and demyelination. Intercellular adhesion molecule-1 (ICAM-1) mediates the extravasation of leukocytes and their accumulation in inflamed tissue. The aim of this study was to evaluate the probable association of ICAM-1 Exon 4 (G241R) and Exon 6 (E469K) gene polymorphisms with circulating levels of sICAM-1 in MS patients (n=78) and consecutive unrelated healthy controls (n=123). Analysis of ICAM-1 polymorphisms was performed by PCR with sequence-specific primers (SSP) and concentration of sICAM-1 in serum was performed by ELISA techniques. No significant differences were detected for allele frequencies of ICAM-1 Exon 4 and Exon 6 in MS patients than in the controls respectively (ns-P > 0.05). Moreover, baseline serum sICAM-1 concentrations to be significantly increased among patient carriers of K allele as compared with the respective non-carriers of these variants (P < 0.001). This study illustrates that K allele of the ICAM-1 codon 469 mutation might contribute to the pathogenesis of MS through increase levels of sICAM-1 and establish inflammation. Our result invites further investigation relevant to understanding the mechanisms underlying the immunopathogenesis of this autoimmune disease.

 

Key words: Polymorphism, intercellular adhesion molecule-1, heterogeneity, single nucleotide polymorphisms (SNP).