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October2013 Vol.50 Issue:      4 Table of Contents
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Interleukin 1 gene Polymorphism and Acute Ischemic Stroke

Rasha H. Soliman1, Walaa A.Kamel1, Manal M.El kattan2,Hanan Helmy,2 Sanaa Abd El-Shafy3

Departments of Neurology, Beni Sueif University1, Cairo University2; Clinical Pathology3,

Beni Sueif University; Egypt

 



ABSTRACT

Background: Elevated Interleukin 1-B (IL1-B) level is considered to be a predictor of ischemic stroke and IL-1b genetic polymorphism is reported to be associated with elevated IL-1b level. Objective: The aim of this work was to study the relation between Interleukin -1b (IL-1b) as well as IL-1b gene polymorphism and ischemic stroke. Methods: Twenty-five ischemic stroke patients and twenty five normal subjects were included in  this study. Patients were evaluated clinically and radiologically. Laboratory investigations, IL-1b assay and genetic testing of IL-1b gene were done for both  patients and control groups.  Results: Serum IL-1b level was significantly high in ischemic stroke patients compared to control subjects and high IL-1b level was significantly associated with D.M, hyperlipidemia, total anterior circulation syndrome (TACI), large sized infarction on CT examination and poor stroke outcome. In human IL-1b-511 polymorphism genotype ,there is no significant difference of IL-1b serum concentration regarding IL-1b-511 gene polymorphism. Conclusion: IL- 1b level is elevated in acute ischemic stroke and it is intimately associated with different vascular risk factors and prognostic factors. Human IL-1b-511 polymorphism did not influence the serum level of IL-1b and did not show any association with ischemic stroke. [Egypt J Neurol Psychiat Neurosurg.  2013; 50(4): 455-461] 

Key Words: Ischemic stroke – Interleukin 1B – Polymorphism

Correspondence to Hanan Helmy, department of neurology, Cairo University, Egypt. Tel.: +201229123430. Email: drhananelgendy76@yahoo.com






INTRODUCTION

 

Stroke is the second leading cause of death and one of the most frequent causes of disability worldwide 1. The incidence of stroke among Egyptians is not accurately known due to lack of reliable surveys. Yet it is generally estimated to be 2.1 per 1000. The prevalence was 5.4 per 1000.  Cerebral  ischemia  constituted  78%  while  cerebral hemorrhage  22%  of  stroke.  Cerebral  ischemia  involved  middle cerebral artery (MCA) in 73.7% and capsular hemorrhage 12% of cases 2.

        There are many evidences that inflammation and immune response play an important role in the outcome of ischemic stroke patients, and they have been associated to larger brain damage. However, on the other hand, these mechanisms might be necessary for the resolution of dead cells and the initiation of repairing mechanisms 3. Central administration of IL-1 exacerbates brain damage, and overexpression of the IL-1 receptor antagonist (IL-1Ra) or blockade of IL-1 converting enzyme activity reduces infarct size dramatically. Clinical studies suggest there is intrathecal

 

IL-1 production early during stroke 4. The fact that increased levels of IL-1β mRNA have been detected in human atherosclerotic plaquessuggests that IL-1 may enhance the local immunoreaction. The activity of IL-1 (mainly IL-1β ) is modulated by IL-1 receptor antagonist (IL-1Ra).The latter is secreted by the same cells secreting IL-1 and acts as an antagonist of IL-1 by blocking the IL-1 receptor. A single nucleotide polymorphism in the promoter region of IL-1β at position −511 resulting in C–T transition influences the protein production, and IL-1β-511T carriers are reported to be higher producers of IL-1β than IL-1β-511C carriers 5.

The aim of this work was to study the relation between Interleukin -1b (IL-1b) as well as IL-1b gene polymorphism and ischemic stroke

SUBJECTS AND METHODS

 

Subjects

The participants were recruited from Neurology Department, Beni-Sueif University Hospital during the period from July 2011 to November 2011.

Twenty five patients (group I) (6 males and 19 females) with   acute   first   ever   ischemic stroke (within first 24 hours of stroke onset) diagnosed clinically and by computed tomography (CT) were included in the study. Patients' age ranged from 45 to 60 years with a mean age of 56.5±4.5 years.

Excluded from the study were patients with hemorrhagic stroke diagnosed by CT, and patients with cerebral embolism of cardiac origin diagnosed clinically and by ECG, and echocardiography. Also, patients with cancer, liver ,kidney and autoimmune disease were excluded. No participants had a history of  myocardial infarction, recurrent stroke or any acute or chronic infection at the time of sampling, no participants had a history of trauma, surgery or on regular anti-inflammatory drugs excluding aspirin.

Twenty five  healthy subjects (group II) (10males and 15 females) were enrolled as control subjects, their age  ranged  from  45  to  60  years  (mean  age  of 54.5±5.3 years). Excluded from this group, subjects with history of stroke or myocardial infarction, rheumatic heart diseases, autoimmune diseases. Diabetic and hypertensive persons or persons with any  acute  or  chronic  infection  at  the  time  of sampling were also excluded.

 

Methods

Patients  were  evaluated  by clinical examination and were clinically classified using Oxfordshire  Community  Stroke  Project Classification (OCSP)8 into lacunar infarction syndrome  (LACI),  total  anterior  circulation infarction syndrome (TACI), partial anterior circulation  infarction  syndrome  (PACI)  and posterior circulation infarction syndrome (POCI).

Assessment of stroke severity and level of impairment using the National Institute of  Health Stroke Scale (NIHSS)9, which is a standardized neurologic   stroke   severity   scale   developed   to quantify stroke patients' deficits in clinical trials. A score of 1-4= minor stroke, 5-15 = moderate stroke,

15-20 = moderate /sever stroke and 21-42=sever stroke.

Assessment of functional outcome using different stroke scales: Modified Rankin Scale (MRS)(10), which is an efficient global functional outcome index after stroke. It is a 7 grade scoring system with 0 corresponding to persons having no symptoms and 6 being dead.

Glasgow Outcome Scale (GOS)11, a  5  point scale that reflects disability and handicap. A score of

1-2 is considered good outcome, whereas a score of

3-6 is considered poor one.      Barthel index(BI)12,a score of 60 or more ,patients are independent for essential personal care and can be considered as good outcome, a score of less than 60 as bad outcome.

The outcome   functional   scales   were   done   for patients one month after stroke onset. Laboratory investigations were done and they included routine laboratory profile and specific laboratory investigations including: (a) quantitative measurement of human IL-1b  in serum by enzyme-linked immunosorbent assay(ELISA),  Normal values of serum Il-1b are 0.00 pg/ml to 3.72 pg/ml .

           b)Genetic profile: DNA gene polymorphisms(one single base  pair) at position-511 promoter region of IL-1b gene were assessed by PCR technique.

 

Computed tomography of the brain was done using the Toshiba Express/XS System, initially and follow-up after 72 hours if needed. The scans were conducted in the axial imaging planes. The axial cuts were  normally at  10  mm.  Size  of  infarction was detected as follows: small infarction: <1 cm, moderate sized infarction: 1-3 cm and large sized infarction: >3 cm.

The control group underwent the same routine and specific laboratory tests (Il-1b) and genetic testing).

 

Statistical Methods

Quantitative data were summarized as means and standard deviations. Categorical data were summarized as percentages. Qualitative data were compared by Chi-square or Fisher' exact tests according to the expected frequencies. Persons Correlation Coefficient, which is a test to measure the strength of the linear relationship between two variables was used. A 5% probability level (p<0.05) was considered statistically significant.

 

RESULTS

 

Hypertension   was   found   in   17   patients (68%), four patients were cigarette smokers (16 %),  TIAs  in  5  patients  (20%)  and  family history of stroke in 1 patient (4%). Hypercholesterolemia was found in 9 patients (36%),hypertriglyceridemia was found in5 patients(20%),low HDL in 12 patients(48%) elevated blood sugar in 9patients (36%) and hyperuricemia in 6 patients (24%).

Clinically LACI syndrome was diagnosed in 4 patients (16%), TACI in 2 patients (8%), PACI in 19 patients (76%) and no patients had POCI syndrome.

Assessment of stroke severity by NIHSS revealed mean of 10.1±8.3 with 22 patients (88%) having good outcome and 3patients (12%) having poor outcome.

Clinical functional outcome scales showed mean MRS of 2.6±1.2 with 19 patients (76%) with good outcome, GOS mean of 2±0.6 with 21 patients (84%) with good outcome, and BI mean of 66.6±23.8 with 17 patients with good outcome.

CT results  showed  13patients  (52%)  had small sized infarction, 7 patients (28%) had medium sized infarction and 5  patients (20%) had large sized infarction.  Specific Laboratory Results:

 

(a)  Serum Interleukin 1B levels (IL-1b):

Elevated serum IL-1b was found in 9 patients (36%) while normal serum IL-1b was found in 16patients (64%). Whereas all subjects in control  group  had  normal  serum  IL-1b  levels. There was a highly significant difference between acute stroke patients and control subjects regarding the mean level IL-1b (p-value <0.01) (Table 1).

 

(b) IL1bgenotyping:

Human IL-1b-511 polymorphism genotype results revealed that (TT allele) was found in 10 patients (40%) and 10 persons of control group (40%), while (CC allele) was found in 10 patients (40%), and  in 5 persons (20%) in control group. The third allele (CT) was found in 5 patients(20%) in group I,and in 10 persons of control group(40). In patients having the homozygous allele TT, the mean IL-1b level was 64.8±104.7 pg/ml , the mean level of IL-1b in patients having CC allele was 20.6±61.5 pg/ml, whereas the mean level in patients having CT allele was 129.6 ±209.1  (Table 2).

 

Relation of IL-1Blevel and risk factors and CT

findings:

 

1-Hypercholesterolemic patients had significantly higher mean level of IL-1b (320 ±10.2 pg /ml than normal cholesterol level patients (p value=0.013).Also patients with high FBS were highly significantly associated with elevated IL-1b (234.5 ±120.2 pg/ml).

 

2- However, gender, smoking, TIAs, HT, hyperuricemia, hypertriglyceridemia, elevated WBCs count did not reach a significant level.

3-According to OCSP: patients with LACI had significantly lower serum level of IL-1b  (1.4±1.1 pg/ml) than patients with either TACI or PACI (345.6±212.1 pg/ml) (42.4±81.5pg/ml) respectively.

 

4- Patients   with   large   infarction   had   highly significant mean level of IL-1b (154.3±210.8 pg/ml) than patients with small and medium sized infarction (36.5±77.5 pg/ml) (Table 3).

 

Correlation study between IL-1b serum level and different laboratory risk factors and outcome scales (Table 4):

1.              There  was  positive  correlation  between  IL- 1b  and  different  laboratory  risk  factors, which reached statistical significance regarding cholesterol level only.

2.     Negative   correlation   between   IL-1b   and HDL serum level(did not reach significant value), negative correlation was present between IL-1b and BI(did not reach significant value).

3.      Also positive correlation was present between IL-1b  level and different assessment and outcome scales(NIHSS,GOS and MRS).Correlation with MRS reached a highly significant value.

 

 

 

Table 1. Serum high sensitivity CRP levels in group I (patients with acute stroke) and group II (Healthy controls)

 

IL-1b

Group I

Group II

P value

Minimum

0.7

0.5

 

 

0.01*

Maximum

495

3.3

Mean ±SD

60.1±120.3

1.5±0.8

IL-1b interleukin 1b      SD standard deviation         

*Significant at p<0.01

 

Table 2. IL-1b levels according to IL-1b polymorphism in group 1(patients with acute stroke)

 

IL-1b polymorphism

Serum IL-1b(Mean±SD)

CC

20.6±61.5

TT

64.8±104.7

CT

129.6±209.1

IL-1b interleukin 1b      SD standard deviation 

 

Table 3. IL-1b levels and size of infarction in group I(patients with acute stroke)

 

Infarction size

Large infarction

Small and medium infarction

P value

IL-1b (Mean±SD)

154.3±210.8

36.5±77.5

0.047*

IL-1b interleukin 1b      SD standard deviation         

*Significant at p<0.01


Table 4. Correlation between IL-1b level and laboratory risk factors and clinical assessment and outcome scales in patients with acute ischemic strokes

Laboratory risk factors and different assessment and outcome scales

r value

P value

 

Cholesterol level

0.5

0.011 *

 

Triglycerides level

0.1

0.614

 

Fasting blood sugar

0.2

0.075

 

HDL

-0.2

0.065

 

LDL

0.1

0.0687

 

Uric acid

0.2

0.085

 

ESR

0.1

0.0751

 

WBCs

0.3

0.051

 

NIHSS

0.1

0.761

 

GOS

0.2

0.63

 

MRS

0.6

0.001 **

BI

-0.2

0.071






ESR erythrocyte sedimentation ,   GOS  Glasgow outcome scale ,  HDL   high density lipoprotein , LDL   low density lipoprotein , MRS    Modified Rankin scale, NIHSS    National institute of health stroke scale, WBCs      white blood cells, BI    Barthel index,  

*Significant at p<0.01

 

 


DISCUSSION

 

There is increasing evidence that inflammation plays an important role in acute ischemic stroke(AIS),indicating important interactions between the nervous and immune systems 13.

       In this study there was a highly significant increase in the IL-1b serum level in the first 24 h after acute ischemic stroke and this was in accordance with some preceding studies 14,15. A finding which can be explained by the fact that ,inflammation plays a central role in all phases of atherosclerosis, from the initial recruitment of circulating leukocytes to the arterial wall to the rupture of unstable plaques, which  results in the clinical manifestations of the disease.IL-1b may  be involved in each of these stages by direct influencing processes like complement activation, apoptosis, vascular cell activation ,lipid accumulation and thrombosis 16.

       On the other hand, Heidi et al 17.concluded that, IL-1b was not elevated in the AIS group.

     Tarkowski et al.18stated that although cytokines are detected in the brain and CSF of patients with AIS and the relevance of measurements in the peripheral  circulation is uncertain.

       Inflammation has a relevant role in the initiation and progression of atherosclerosis 19. however, it can also play a primary role in thrombosis development by activating the coagulation process  20.

     Patients with hypercholesterolemia and high blood sugar had respectively (significantly, highly significant) higher levels of IL- 1b   pointing  to  a  relation  between   lipids, diabetes and inflammation. This was in accordance with previous studies 22,23.

      This was in accordance with epidemiologic studies done by Alexanraki et al 21 that  have been demonstrated strong relationship between inflammatory markers and metabolic disturbance ,whereas inflammation has been considered as a "common soil" between these clinical entities and type 2 diabetes.

     Ehses et al.24established a study that IL1b affects both beta cell functional mass and insulin sensitivity in type 2 diabetes . In accordance with these observations,IL-1b expression is shown to be increased in islets from type 2 diabetic patients 25.

       Our study revealed that lacunar stroke patients exhibited a highly significant lower level of IL-1b in comparison with subjects with non-lacunar strokes. This was in accordance with previous studies done by (Licata et al.)16 Tuttolomondo et al.27. Our finding is possibly related to a lower extension of lacunar infarcts with a lower grade of recruitment of leukocytes into infarct area and consecutively with a minor release of bioactive substances e.g. ROS, granular enzymes or cytokines that induce damage to neural cells 26.

       In this study, a statistically significant relation between elevated IL1b level and bad outcome of BI and GOS, these data were in agreement with others 27,28.

Patients with large infarction had a significantly higher IL-1b level than those with small and medium sized infarction. This was in accordance with Chamorro and Hollenbeck  27that demonstrated that elevated CSF and blood levels of IL-1b correlates with larger brain infarcts.

  This study revealed that the mean IL-1b level was higher in CT allele polymorphism than that in CC or TT allele in stroke patients. but the CT allele (the least common allele) was found in 20% of patients, while CC,TT allele were found in 40% in each .On the other hand the CT allele was found in 40% of control group, so the significant difference between the IL-1b level in patient group and control group cannot be explained on the genetic basis.

       This was supported by other previous studies 29,30,31 who found that ,there was no significant difference of IL-1b serum concentration regarding IL-1b-511 gene polymorphism.

        On the other hand, Lai et al.31 revealed that C to T single base polymorphism in the promoter of IL-1b gene (C-511-T) have been reported to affect the levels of IL-1b .It is also reported in several studies that these polymorphisms are associated with the susceptibility to cardio-cerebral vascular disease.

        Nemtz,34stated that a single nucleotide polymorphism in the promoter region of IL-1b at position -511 result in C-T transition influences the protein production and IL-1b -511 T carriers  are reported to be higher producers of IL-1b than IL-1b -511 C carriers.

These conflicting data suggests  that,  genetic and  environmental determinants, each  importantly contribute to the vascular risk associated with inflammation. Although the mechanism for a direct effect is unclear, so, it  remains possible that this polymorphism is  in  strong  linkage  disequilibrium with a polymorphism in a distal regulatory element not within the region scanned for polymorphisms.

Conclusion:

Elevated IL-1b  level is significant in acute ischemic stroke and  associated with  multiple  risk and prognostic factors however, its genetic polymorphism did not influence its level.

 

[Disclosure: Authors report no conflict of interest]

 

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الملخص العربي

 

التعدد الجيني للانترليوكين -1 في السكته الدماغيه الحاده

 

تهدف هذه الدراسة إلى توضيح العلاقة بين مستوى الانترليوكين 1 ب في الدم والتعدد الشكلي الجيني له وبين السكتة الدماغية الحادة. هذاوقدأجريت هذه الدراسة على خمس وعشرون مريضا يعانون من الجلطة المخية الحادة واشتملت على6 رجال و19سيدة تراوحت أعمارهم بين45إلى60سنة بمتوسط  4.5±56.7سنة. كما اشتملت هذه الدراسة أيضا على خمس وعشرون آخرون من الأصحاء كمجموعة مقارنة بمتوسط عمري 54.55.3±.تم تقييم المرضي اكلينيكيا مع عمل اشعه مقطعيه علي المخ-تافحوصات المعمليه الروتينيه-قياس مستوي الانترليوكين 1 ب بالدم-والتعدد الجيني لجين-511 للانترليوكين 1 ب لكل من المرضي والاصحاء.

هذا وقد أظهرت النتائج التالي:نسبة القياس في المرضى أعلى من الأصحاء وهذه النتيجة ذات دلالة إحصائية.مرضى السكر و ارتفاع الكولسترول بالدم كانت لديهم نسبة الانترليوكين 1 أعلي وهذه النتيجة ذات دلالة إحصائية.هناك علاقة ذات دلالة إحصائية بين نسبة الانترليوكين 1 ب بالدم بالمرضى والجلطة المخية كبيرة الحجم.المرضي الذين كان لديهم ناتج سيءفي مقياس جلاسكو ومقياس بارثل كانت لديهم نسبة الانترليوكين 1 ب أعلى وهذه النتيجة ذات دلالة إحصائية.أما بالنسبة لمقياس المعهد الدولي للصحة للسكتة الدماغية فإن نسبة الانترليوكين 1 بفي المرضى الذين لديهم إعاقة شديدة كانت أعلى ولكن لم تصل إلي دلالة إحصائية.

المرضى الذين كانت لديهم جلطة مخية لاحتباستام في الدورة المخية الأمامية تبعا لمقياس أكسفوردشاير لديهم نسبة الانترليوكين 1 ب أعلى نسبة وذات دلالة إحصائية عالية.تم دراسة التعدد الشكلي الوراثي لجين511 للانترلوكين 1 ب في المرضى والأصحاء وقد وجد أن:الصفة الجينية TTوجدت في40 % من المرضى والاصحاء ووجدت الصفةالجينيةCC في 40% من المرضي وفي 20% من الأصحاء بينما وجدت الصفة الجينية CTفي 20%من المرضي و40% من الأصحاء.كماوجد أن في المرضى ذوي الصفة الجينية CT نسبة الانترليوكين 1 ب كانت أعلى من المرضى أصحاب الصفات الجينية CC-TT



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