The correlation between IFNγ serum level and IFNG+874 SNP in a multiple sclerotic Iraqi patients

العناوين الأخرى

العلاقة بين المستوى المصلي ل IFNγ و التغاير الوراثي احادي النكليوتيدة ل IFNG +874 عند مرضى عراقيين بالتصلب العصبي اللويحي المتعدد

المؤلفون المشاركون

al-Nasiri, Milad Abd al-Salam
Adhiah, Ali Husayn
Salman, Ihab Dawud

المصدر

Iraqi Journal of Science

العدد

المجلد 57، العدد (sB) (31 ديسمبر/كانون الأول 2016)، ص ص. 321-327، 7ص.

الناشر

جامعة بغداد كلية العلوم

تاريخ النشر

2016-12-31

دولة النشر

العراق

عدد الصفحات

7

التخصصات الرئيسية

الأحياء

الموضوعات

الملخص EN

Multiple sclerosis (MS) is a neurodegenerative autoimmune disease causes a demyelination in neuronal axon and multifocal lesions in especially white matter.

Genetic, epigenetic and environmental factors play a pivotal role in the pathogenesis of MS.

IFNγ is a proinflammatory cytokine that enhances Th1-cell immune response upon infection and is considered as exacerbation factor in relapsing-remitting MS (RRMS) patients.

The current study aimed to find the association between serum level of IFNγ and single nucleotide polymorphism (SNP) genotypes/alleles at locus +874 of IFNG gene.

Sixty eight Iraqi Arab Muslim patients infected with RRMS were enrolled in this study and they were categorized into two group: IFNβ pre-medicated and IFNB post-medicated patients.

Twenty Iraqi healthy individuals were chosen as control group.

ELISA assay was used to measure IFNγ serum level and sequence specific primers –polymerase chain reaction (SSP-PCR) technique was used for genotyping IFNG+874 SNP.

The results showed insignificant difference between IFNβ pre-medicated and IFNβ post-medicated patients, while there was a significant decreased ( P=0.015) mean serum levels in RRMS patients pre-medication and post-medication RRMS patients as compared to control group (68.8 ± 3.3 and 68.5 ± 4.46 vs.

91.8 ± 10.5pg/ml( respectively.

The results demonstrated that there was nonsignificant difference between observed and expected genotype frequencies of IFNG gene SNPs at position +874.

In addition, there was insignificant variation between patients and controls in the distribution of these genotypes and alleles.

The results also revealed that there was no impact of IFNG gene SNP at locus +874 on the serum level of this cytokine in RRMS patients.

Meanwhile, a significant increase of control group serum level corresponding TT genotype compared to that corresponding AA genotype (114.8±24.03 vs.

66.67±10.87) (P = 0.004 pg/ml ( respectively.Furthermore,it was observed that a significant decrease (p=0.042;p=0.08) of patients’ IFNγ serum level corresponding both AT and TT genotypes as compared to those in control group (64.9±4.33 vs.

90.42 ± 12.58, 77.72± 7.54 vs.

114.8±24.03 , pg/ml respectively.

Briefly, the results indicated that IFNG+874 SNP has no effect on serum level of RRMS Iraqi patients and also has no effect on MS risk.

The low levels of IFNγ in RRMS patients may be attributed to the remitting state of the patients.

نمط استشهاد جمعية علماء النفس الأمريكية (APA)

al-Nasiri, Milad Abd al-Salam& Salman, Ihab Dawud& Adhiah, Ali Husayn. 2016. The correlation between IFNγ serum level and IFNG+874 SNP in a multiple sclerotic Iraqi patients. Iraqi Journal of Science،Vol. 57, no. (sB), pp.321-327.
https://search.emarefa.net/detail/BIM-762589

نمط استشهاد الجمعية الأمريكية للغات الحديثة (MLA)

al-Nasiri, Milad Abd al-Salam…[et al.]. The correlation between IFNγ serum level and IFNG+874 SNP in a multiple sclerotic Iraqi patients. Iraqi Journal of Science Vol. 57, no. (sB) (2016), pp.321-327.
https://search.emarefa.net/detail/BIM-762589

نمط استشهاد الجمعية الطبية الأمريكية (AMA)

al-Nasiri, Milad Abd al-Salam& Salman, Ihab Dawud& Adhiah, Ali Husayn. The correlation between IFNγ serum level and IFNG+874 SNP in a multiple sclerotic Iraqi patients. Iraqi Journal of Science. 2016. Vol. 57, no. (sB), pp.321-327.
https://search.emarefa.net/detail/BIM-762589

نوع البيانات

مقالات

لغة النص

الإنجليزية

الملاحظات

Includes bibliographical references : p. 326-327

رقم السجل

BIM-762589