IBN AL- HAITHAM J. FO R PURE & APPL. SC I. VO L.23 (3 ) 2010 Levels of interleukins 6 and 8 in Psoriatic patients serum M. N. Iqbal College of Medical & Health Technology, Baghdad. Abstract R ecent p rogress in the underst anding of p soriasis has shown that the regulation of local and sy stemic cytokines p lays an imp ortant role in its p athogenesis. Different st udies evaluated the association of serum levels of some p roinflammatory cytokines invivo and their correlation with severity of psoriasis. Eighty cases of psoriatic p atients had been st udied. Patients were divided into mild p soriasis group (30) and sev ere p soriasis group (50) accordin g to severity , and (30) apparently healthy individuals ware used as acontrol group . Sera samples of all group s were collected from all indiv iduals for the estimation levels of interleukins (IL-6 and IL-8). All mean values sera levels (IL-6 32.004 pg/ml and 17.579 p g/ml for IL-8) of p atients were significantly high er than those of controls (12.640 and 8.860 pg/ml for IL-6and IL-8 resp ectively). There was a high si gnificant in sera levels of IL-6 and IL-8, in comparion with disease sev erity . The levels of I L-6 and IL-8 wer e significantly higher in severe p soriatic patients t han thos in mild type. Furthermore, there was a p ositive correlation between the lev els of IL-6, and I L-8 amon g the samples of p soriatic patients. T he measurements of serum levels of these cy tokines may be objective p arameters for the disease severity . Key words: IL-6, IL-8, Psoriasis Introduction At present, the researches of psoriasis are dominated by the hypothesis that it is an immunological disorder described by abnormal keratino cytes proliferation mediated through T lympho cytes [1]. Autoimmun e disorders and inflammatory reaction are currently segregated into cell – mediated Th1 or Th2 categories . Psoriasis is associated with an overexpress ion of proinflammatory cytokines produced by Th1 cells and relative under expression of Th2 cytokines [2].Cytokines are small, bio logically high ly active proteins that regu late the growth, function, and differentiation of cells and help steer the immune response and inflammat ion [3]. Interleukin 6 (IL-6) is a pleiotropic cytokine. Among its characteristic actions are regulation of express ion of other cytokines , induction of proliferation, d ifferentiation of normal and malignant cells, and inhibition of tumor growth. IL- 6 is also regarded as a major inducer of the acute-phase response [4]. Intrleukin 6 is a co mpo nent of normal human skin and it was immun olog ically detected in basal keratino cytes , endothelial cells, many of mon onuclear cells, fibroblas ts, and sudoriparous ducts. Interleukin 6 has been suggested to function as an autocrine mitogen in psoriatic epidermis. In psorias is, intense labeling of the cytoplasm in the vicinity of keratinocytes membranes was detected in the epidermal layers and other skin appendages [5]. Interleukin-8 (IL-8) is probably the best-known member of the family of chemokines [6]. Experimental data documented its role within a cas cade of infla mmatory events. These are focused and amplified by the action of IL-8 by local attraction and activation of different IHJPAS IBN AL- HAITHAM J. FO R PURE & APPL. SC I. VO L.23 (3 ) 2010 leukocyte subsets - prominently neutrophilic granulocytes and lymphocytes [7].Increas ed IL-8 level in blood have been demonstrated in a number of systemic inflammatory disorders [6]. The role of circulating IL-8 in ps oriasis, however, has no t been adequately add ressed in the past. The aim of the present study is to evaluate, IL-6 and IL-8 levels in the serum of ps oriatic patients according to disease activity. Materials and Methods This st udy has been app roved at the consulting center of allergy and asthma – Baghd ad. It was conducted in the period between October 2008-M ay 2009. Patie nts and controls Consecutive p atients with p soriasis who had not received any p rior local or sy stemic treatment within two months were included in this st udy . The diagnosis was mad e clinically , based on characteristic p laque-ty p e p soriatic lesions. Patients with erythrodermic, p ustular, and only p almoplantar forms of p soriasis, and p atients with p soriatic arthritis were excluded. The st udy comp rised (80) p atients (48 females and 32 males) with p soriasis who attended to center of allergy and asthma. Patients were divided into two groups accordin g to the severity of their psoriasis; the severity of psoriasis was assessed by the Psoriasis Area and Sever ity Index (PASI) for each p atient. 30 cases wer e diagnosed as mild p soriasis (p revalence = 40%) and 50 case were diagnosed as severe p soriasis (p revalence = 60%). The mean age of p soriasis cases in gener al was (35) y ears old. In addition a control group consisted of (30) healthy , their mean age was (35) y ears old, un p soriatic volunteers with no family history of p soriasis. Blood and urine wer e collected from both p atients and controls for routine laboratory invest igations including blood sedimentation rate, and blood cell counts. Se rum Venous blood samples (5–10 mL) were taken in vacutainer tubes under sterile conditions from p atients and controls between 09–11 am. Serum was obtained fro m freshly drawn, rapidly centrifugated. Serum was quick ly frozen and st ored for p rocessing. Cytokines detections Sera IL-6 and IL-8, levels were measured by (enzy me-amp lified sensitivity immunoassay (EASIA) k its technique, revised by Biosource Europe. These assay s detected only human cytokines and the minimum detectable concentrations were 1.1p g/mL for IL-6 and 1.9pg/mL for IL-8. S tatistical Analysis: The data were analy zed using the st atist ical p ackage for social science (SP SS) 10.0 for Windows p rogram on the comp uter. The suitable st atist ical methods were used in order to analy ze and assess the results, t hey include the followin gs: Descr iptive st atistics: Summary st atistic of the readings distribution (mean, SD, SEM , minimu m & maximu m) and Graphical p resentation by (Scatter –chart). Inferential st atist ics were used to accept or reject the statistical hyp otheses; they include Student test (t-test), least significant differences (L SD) and Pe arson Correlation (r).The st atist ical si gnificance was a ccepted as (P value < 0.05 &<0.01) [8]. Results The results p resented in this research were based on total of blood samples collected from (80) p soriasis p atients and (30) healthy control individuals. The differential count for leukocytes revealed a characteristic blood eosinophilia among all group s of p atients, that significantly differs from control group (P<0.05).T he p resent data showed, a significantly differences in the mean p ercenta ge of neutrop hils of mild group comp ared IHJPAS IBN AL- HAITHAM J. FO R PURE & APPL. SC I. VO L.23 (3 ) 2010 with the control group , while total p soriatic group did not showed any differences (table- 1). Se rum levels of IL- 6 & IL- 8 The mean, minimum and maximum values of the serum levels of interleuk ins IL-6 and IL-8 of the st udied group s and statistical results are p resented in (table -2). The mean value levels of IL-6 of the p atients were significantly higher than those of the control (32.0 p g/ml and12.64pg/ml) resp ectively at (p < 0.01).The serum IL-8 lev els of p atients were sign ificantly higher than those of controls (17.75 p g/ml) and (8.86 p g/ml) resp ectively at (p <0.01).Table ( 3 ) shows , the mean concentrations of IL-6 & IL-8 wer e high er in sev ere p soriatic group ( 39.24 & 20.48 p g/ml resp ectively ) than in mild p soriatic patients ( 20.98 and 13.152 p g/ml) with higher si gnificantly at p < 0.01 , while the levels of I L-6 &IL-8 in mild p soriatic group showed no significant differences as comp ared with healthy control group ( p > 0.05 ). Correl ation between sera levels IL - 6 and IL- 8 among psoriati c patients. Pearson Correlation has b een app lied to st udy the correlation between lev els of (I L-6) and (IL-8). The results are list ed in Table (4) and figure (1). A p ositive correlation between IL-6 and IL-8 amon g the samples of psoriatic p atients was shown; the sera IL-6 levels were increased with t he increase of sera I L-8 levels in the psoriatic individuals. Discussion The present work revealed that bot h sexes were affected by p soriasis disease, the high er p ercentage of females than males were infected with disease with no significant differences. Recent st udies have revealed that sex hormones manifest a variety of biolo gical and immunological effects in the skin, p regnancy, menst ruation and the menop ause modulate the natural course of psoriasis, indicating a female hormone induced regu lation of skin inflammation. Estrogen invitro down regulates the p roduction of the neutrop hil, type1 T-cell and macrophage att racting chemokines by keratinocy tes, and supp resses IL-12 p roduction and antigen p resenting cap acity while enhancin g anti-inflammatory IL-10 p roduction by dendritic cells. These data indicate that estrogen may att enuate inflammation in p soriatic lesions [9]. The variations between the p resent results comp aring with recent studies may be related to t he differences in sample size, to t he sp ecific morp hological structure of their skin, or the sp ecific Iraqi nature which increased the st ress in the subjective nature and that related to adverse life events. The diagnost ic f eatures may not all be p resent at the same time in every case and ar e some times obscured or evanescent [10, 11]. Eosinophil is a characterist ic of severe and mild cases p soriasis and correlated with skin inflammation [12] .The Eosinop hil p ercentage of current st udy revealed a characterist ic blood eosinophilia, amon g all group s of psoriatic p atients. They significantly differ from control group in accord with [13] who st ated that p erip heral eosinophilia se ems to be associated with severe forms of p soriasis. This finding may suggest that the eosinophils have si gnificant roles in the p athogenesis of p soriasis. In recent studies, it has been documented that the eosinophile cells p lay active role in many kinds of inflammatory disorder, increasin g in number of circulating eosinophils is due to increasing release of eosinophils from bone marrow, the mediators which are involved in this p rocess are Granulocy te M acrop hage-Colony Stimulating Factor (GM -CSF), IL-3 and more selective for eosinophils IL-5 [14]. In addition, these growt h factors are p otent activators for eosinophils, acting at sub nanomolar concentration [15]. However, some of p soriatic p atients had normal eosinophil cell numbers in their p erip heral blood and it is not correlated with score severity skin of p soriatic patients. T he change in eosinophil number might be a result rather than a cause of the disease. It can be concluded fro m these results that the increase in eosinophil cell counts is IHJPAS IBN AL- HAITHAM J . FO R PURE & APPL. SC I. VO L.23 (3) 2010 correlated with severity of the disease. Finally this result refered that t he psoriasis is one of aller gic diseases app eared by its cap acity to st imulate delayed mediated cells hyp ersensitivity which exp ressed by an increase in the production of the eosinop hils. T he results of p resent study are similar to [16] who noted a sign ificantly increased nu mber of leukocytes in inflammatory skin and psoriasis p atients while the results were in a disagr eement with the st udy of [17] who rep orted that mild psoriatic p atients had significantly decreased in mean of leukocytes comp ared with severely group . Finally this result reinforces that t he psoriasis is a common and recurrent skin disorder, characterized with inflammation. Hist ologicaly psoriasis is characterized by marked keratinocy tes hyp erp roliferation,adense inflammatory infiltrate consisting of T cells and neutrop hils, and vascular d ilatation and p roliferation. The p rimary defect in psoriasis p atients was believ ed to be abnormal epidermal cells p roliferation [18]. The very early lesion of p soriasis is characterized by an inflammatory infiltrate of mononuclear cells in the upp er dermis with only min imal changes in the epidermis. The sy st emic effects of circulating cytokines may p lay an imp ortant role in the induction of epidermal cell p roliferation. It was p rop osed that in normal skin there could be an interaction between the epidermis and circulating T cells. Cy tokines are small, biologically highly active p roteins that regulate the growt h, function, and differentiation of cells and help steer the immune resp onse and inflammation [11], Keratinocytes secrete a number of cytokines and chemokines that either activate or supp ress immune resp onses [19]. However, p recise mechan ism of their involvement in p soriasis remains un clear. Any local or sy st emic st imulus may st imulate keratinocy tes cytokines p roduction [20]. The pattern of cy tokine exp ression suggests that Thl cells may mediate or maintain d isease, [21]. The p resent data confirmed the IL – 6 one of the p roinflammatory cytokines is influenced in serum of psoriatic p atients [5, 11&22] and contrary to other tested Th2 typ e cytokine IL – 6, had sera levels comp arable with normal controls [23].M oreover, the present results showed significant differences in IL – 6 sera lev els among st udied p atients group s accordin g to the sever ity of disease. Present results are in line with p revious rep orts which found that IL-6 was shown t o be elev ated in serum of patient with active dise ase [24, 25]. It had been rep orted that IL-6 elevation p ositively correlated with p soriatic Assessment and Sever ity Index Scores. [25, 26] Interleukin 6 mediates T-cell activation, st imulates p roliferation of keratinocytes, and at the beginnin g of acute inflammation, med iates the acute phase resp onses [11]. Int erleukin 8 (IL-8) is the best - known ch emokines. Its action is greatly enhanced by IL-1 and TNF-α. Interleukin 8 exerts a very strong chemotactic activity towards neutrop hils [20]. Gearin g et.al, [27] st udied different cytokine levels, which were, IL-2, IL-4, IL-6, IL-8 and GM -CSF in aqueous extracts of st ratum corneum from p soriatic lesions and normal heel. They found that IL-8 was the only biologically active cytokine to be elevated in psoriatic lesional extracts. In t he present st udy , serum IL- 8 was sign ificantly increased in p atients group s when comp ared with healthy control. M oreover it was increased significantly in severe p soriatic comp ared with mild p soriatic and healthy control group s. While the differences between mild group and healthy control was insignificant. The p revious results did not found correlation between serum IL-8 levels and p soriasis severities and st ate of disease PASI [28]. Different data p ointed out increase serum IL-8 and IL-6 in p soriasis [29]. So me of the rep orts also demonst rated that either lesion al or serum lev els of these cytokines reflect to some extent disease activity and treatment [30]. Shimizu et.al, [31] reported p soriatic skin disease p atients had increased serum levels IL-8, and it's incr easin g was p ositively correlated with disease activity . Also [23] they found increase of IL-8 levels in p soriatic p atients (24.4p g/ml) versus normal controls (3.6p g/ml) and p ositively correlated with degree of erythema. M any st udies indicated that IL-8 may be involved in the p athomechanism of p soriasis. In fact, data currently available suggest ed that this cytokine exerts a critical ro le as a p otent chemoattractant for neutrop hils and T lymp hocy tes, as well as a factor p rompting IHJPAS IBN AL- HAITHAM J. FO R PURE & APPL. SC I. VO L.23 (3 ) 2010 keratinocy te p roliferation [19].Interleukin 8 is known as chemotactic factor for neutrop hils and, by an indirect mechanism induces neutrop hil degranulation [24]. As neutrop hils are present in the epidermis of t he psoriatic lesions, it is p ossible that IL-8 aids in their recruitment and thus contributes t o the erythema- while the kin etics of I L-8 in the serum of p atients with psoriasis are not known, one could p resume that IL-8 could be a good index for the inf lammatory p rocess and a crucial element in the cellular activation of p soriasis [23]. Several cytokines are in creased in psoriasis, either at local or sy st emic level or both including Tumor Necrosis Factor alp ha (TNF-α) IL-2, IL-6 –IL-8, Interferon gamma (IFN- γ), and Transforming Growth Factor alp ha (TGF- α) which are regarded as hallmark, cytokines in p soriatic cy tokine network [32]. Cytokines p lay an imp ortant role in the pathogenesis of p soriasis [23]. When measuring cytokines levels in serum, it is not p ossible to determin e the or igin of these cy tokines, t he serum cy tokine concentrations are altered by several p rocesses like the production, tissue or cellu lar d eposition, degr adation, and elimination of these molecules; furthermore other tissue sources of cytokine p roduction might exist beside the cir culatin g T-cells and the origin of circulating cytokines in blood serum in p soriatic p atients is not clear, to achieve the cytokine concentration that can induce biolo gical resp onses at distant skin lesions, huge amounts of free cytokines that induce gener alized inflammation are requir ed, thus, the receptors on p soriatic keratinocytes may be more sensitive to these cytokines [11]. In p resent study a p ositive correlation between ser a lev els of IL-6 and IL-8 were d emonst rated that IL-8 could be regarded as an additional a p art from IL-6, indicator of p soriasis activity . It is difficult to draw conclusions and very difficult to comp are data obtained in different laboratory conditions. It could be argu ed that p lasma levels of examined cytokines were already p erformed and p ublished a few times but one has t o bear in mind also the fact t hat cytokine evaluation r esults may vary due to differ ent assay s, individual variation in the st age of disease, d emo graphic differences, and coexist ing p athologies [33]. Unt il other inflammatory skin diseases are studied, we cannot sp eculate on the sp ecificity of these results, and further invest igations will be required to define the role of serum p roinflammatory cy tokines in the p athogenesis and their correlation with clinical severity of p soriasis. Re ferences 1.Chamian,F.& Krue ger,J.G. (2004) Psoriasis vulgaris an interplay of T ly mp hocytes, dendritic cells, and inf lammatory cytokines in pathoge-nesis. Curr. Op in.Rheumatol.16(4):331-337.(1) 2.Gudjonsson, J.E.,Johnston, A.,Sigmundsdottir,H. & Valdimarsson, H. (2004)Immunop athogenic mechanisms in p soriasis clin. Exp .Immunol. 135(1):1-8.(2) 3.ThomsonA.T heCytokinesHandlbook (1998).3 rd ed. NewYork,NY: Academic Press. 4.Borden,E.C.& Chin,P. (1994) Interleukin-6:a cytokine with p otential diagnost ic and therap eutic roles. The J. of Laboratory and clinical M edicine. 123(6):824-829. 5.Zalewska,A.,Glowacka,E.,Wyczolkowska,J.,Tchorzewski,H.,Narbutt, J. & drzejowska, A. (2006) Interleukin 6 and 8 lev els in Pl asma and fibroblast culture in p soriasis. M ediators of Inflammation:1-6. 6.Baggiolini,M ., Dewald B. &M oser B. (1997) Human chemokines: An up date. Annu Rev Immunol 15:675-705. IHJPAS IBN AL- HAITHAM J. FO R PURE & APPL. SC I. VO L.23 (3 ) 2010 7.Schroder,J.M . (1997) Identification and st ructural characterization of chemokines in lesional material of p atients with inflammatory skin disease. M ethods. Enzy mol. 288:266- 297. 8.Sorlie, D.E. (1995) Epidemiology , examination and board review. First ed. Norwalk, Connecticut, Ap p leton and Lange: 47-88. 9.Watanabe, S. (2008) "Regulatory roles of sex hormonal in cutaneous biology and immunology " J. Dermatological Science. 38(1):1-7. 10.Barker, J.N. (1999)"Genetic asp ects of p soriasis". Clin. Exp . Dermatol. 26:321. 11.Arican, O.; Sasmaz, S.&Ciragil,P. (2005)"Serum Levels of TNF-alp ha, INF-gamma,IL- 6,IL-8,IL-12,IL-17,and IL-18 in p atients with Active Psoriasis and Correlation with disease severity ". M ediators of inflammation.5 (2005) 273-279. 12.Schroder, J.M . (1998).Chemokines and eosinophils. An article in a book series‘’Progress in inflammation research Brikhauser Verlag Basel. Swfierland. 13.M ansur,F, Goktay ,S, and Yasar,P.(2007) Peripheral blood eosinop hilia in association with generalized p ustular and erythrodermic p soriasis . Journal of the European Academy of Dermatology and Venerolo gy (Online Early Articlles).M unksgaard International Publishers Ltd. 14.Koning, H. (1996) T and B cells activation in childhood allergy : Acrose – sectional and st udy of cytokines and immunoglobulins Netherlands. 15.Dubois, G.R.; Brui Jnz eel, K.CA. and Bruui Jnzeel, P.L. (1994) IL-4 induces chemotaxis of blood eosinop hils from normal indviduals.J.Invest . Dermatol.102:843-846. 16.Walker, C; Kagi, U.K., Ingold, p .; Braun, p .; Blaser, K.; Koomen, C.A.;and Wuthrich, B.(1993)A t op ic dermatitis: Correlation of p erip heral blood T-cell activation, eosinop hilia and serum factors with clinical severity , din. Exp . Allergy .23:145-153. 17.Al-kasmie,S F. (2002) Study of some Immunological and Biochemical Asp ects of Psoriatic p atients. M .Sc thesis College of Science, Al- M ust ansiriy a University . 18.Fry L. (1988) Psoriasis. Br J Dermatol.119 (4):445–461. 19.Bonifati,C.andAmeglio,F.(1999)Cy tokines in p soriasis. Int. J. Dermatol.38 (4):241–251. 20.Nickoloff, B.J, Karabin, G.D, Barker, J.N., Gri¤ths, C.E.M ., Sarma,V., and M itra, R.S.(1991) Cellular localization of interleukin-8 and its inducer, tumor necrosis factor-alp ha in psoriasis. Am. J. Pathol.138(1):129–140. 21.De Rie,M .A, Goedkoop , A.Y., Bos, J.D.(2004) Overview of p soriasis. Dermatol. Ther.17 (5):341–349. IHJPAS IBN AL- HAITHAM J. FO R PURE & APPL. SC I. VO L.23 (3 ) 2010 22.Abanmi, A., Al Harthi, F.,Al Agla, R., Khan, H.A/,and Tariq, M .(2005) Serum levels of p roinflammatory cytokines in p soriasis p atients from Saudi Arabia. Int .J. Dermatol.44 (1):82–83. 23.Jacob, S.E., Nassiri, M ., Kerdel, F.A., Vincek, V. (2003) Simultaneous measurement of multiple Th1 and Th2 serum cytokines in p soriasis and correlation with disease severity . M ediators Inflamm.12 (5):309–313. 24.Pietrz ak, A., Koz iol-M ontewka, M ., Lecewicz-T orun, B., Krasowska, D. (2000) Is there any correlation between the total number of neutrop hils in p lasma and concentration of interleukin-8 in p soriatic patients? M ed Sci. M onit.6: 867-870. 25.Szepietowski J.C., Bielicka, E., Nockowski, P., Noworolska, A.,and Wasik, F.(2000) Increased interleukin-7 levels in the sera of p soriatic p atients: lack of correlations with interleukin-6 levels and disease intensity . Clin. Exp . Dermatol.25: 643-647. 26.Gomi, T., Shiohara, T., M unakata, T., Imanishi, K., Nagashima, M . (1991) Interleukin -1 alp ha, tumor necrosis factor alp ha, and interferon gamma in p soriasis. Arch. Dermatol. 127: 827 -830. 27.Gearing A.J., Fincham N.J.and Bird, C.R.(1999) Cy tokines in skin lesions of p soriasis. Cy tokine.2 (1):68–75. 28.Sticherling,M .,Sautier,W.,Schroëder.J.M .andChrist op hers,E.(1999)Interleukin-8 Plays its Role at Local Level in Psoriasis Vulgaris Acta Derm Venereol (Stockh) 79: 4-8 29.Yoshinaga,Y.,Higaki,M.,Terajima,S.,Funato,T.andKatayama,I.(1995)Detection of inflammatory cytokines in psoriatic skin. Archives of Dermatolog ical Research.287 (2):158–1 64. 30. Biasi, D., Carlett o, A.,and Caramaschi, P. (1998) Neutrop hil functions and IL-8 in p soriatic arthritis and in cutaneous p soriasis. Inflammation. 22(5):533– 543. 31. Shimizu,T .,Nishihira,J.,M izue,Y.,M izut ani, H.,and Ohmoto, Y.(2001) High macrophage migration inhibitory factor (M IF) serum levels associated with extended p soriasis.J Invest. Dermatol. 116: 989-990. 32. Schon, M .P., Boehncke, W.H. (2005) Psoriasis. The New England Journal of M edicine. 352(18):1899–1912. 33. Ameglio,F.,Bonifati,C.,Pietravalle,M .,and Fazio, M.(1994) Interleukin- 6 and tumour necrosis factor lev els d ecrease in the suction blister fluids of p soriatic p atients during effective therapy .Dermatology 189(4): 359–363. IHJPAS IBN AL- HAITHAM J. FO R PURE & APPL. SC I. VO L.23 (3 ) 2010 Tabl e -1: Baseline clin ical an d dem ographi c fin dings of stu dy groups Subjects Charact eristics Mild group N=30 Sever group N=50 T otal group N=80 Control group N=30 Age R ange (mean ) years 12-40 (25) 12-70 (43) 12-70 (34) 12-65 (35) Sex (female/male) 22/8 26/24 48/32 20/10 Percentag e o f frequ ency 40% 60% 100% --------- Neutrophils percent age Range Mean. ± SD * (57-61.3)% 58.8  3.5 * (48.7-56)% 53  3 (48.7-61.3)% 55.9  3.3 (48-59.3)% 54  3.56 Eosinophils percentage Range Mean. ± SD (4 -7)% 5.75  0.63 (2 -12)% 6.5  0. 735 * (2 -12)% 6.12  0.623 * (2 – 4)% 2.7  0.94 *significant differences at (p< 0.05) Table (2) Se ra levels of IL6&IL-8( pg/ml) i n a study groups Table (3) Se ra levels of IL-6 & IL-8amongpsoriati c patients. *NS = Non significant (p >0.05) , HS= High sign ificant (p >0.001) Parameters Study groups N. Mean± Std.error Range t-test(P-value) IL-6 Healthy control 30 12.640 ± 2.176 1.5 -40.5 .000 (p<0.01) Psoriatic patients 80 32.004 ± 2.521 3.0 -70.9 IL-8 Healthy control 30 8.860 ± 1.212 1.0-20.5 .000 (p<0.01) Psoriatic patients 80 17.579 ± 1.213 .0 - 42.3 Parameters Statically parameters Psoriatic groups Healthy control (c) LSD Mild (a) Severe (b) P-value Sig IL-6 Range Mean S. error 3.0 -60.7 20.987 3.747 6.5 -70.9 39.243 2.793 1.5 - 40.5 12.640 2.176 (a)-(b)=. 000 (a)-(c)=.084 (b)-(c)=.000 HS NS HS IL-8 Range Mean S. error 0. – 30.5 13.152 1.648 4.5 – 42.3 20.489 1.517 2.0- 20.5 8.860 1.212 (a)-(b)=. 001 (a)-(c)=.079 (b)-(c)=. 000 HS NS HS IHJPAS IBN AL- HAITHAM J. FO R PURE & APPL. SC I. VO L.23 (3 ) 2010 Table (4): Correlation between sera levels of (IL-6 & IL-8). Fig (1): S catter plot of correl ations between se ra levels of (IL –6 & IL-8) among patie nts Correlations .852 .000 HS Pearson Correlation (r) P-value Sig. Ser um I L- 6 (Pg/ml) Serum IL-8 (Pg/ml) Seru m IL-6 (Pg/ml) 80757065605550454035302520151050 S er u m I L -8 ( P g /m l) 50 45 40 35 30 25 20 15 10 5 0 IHJPAS 2010) 3( 23مجلة ابن الھیثم للعلوم الصرفة والتطبیقیة المجلد لكل من االنترلوكین السادس والثامن لدى مرضى المستویات المصلیة ةالصدفی میادة نوري اقبال بغداد،كلیة التقنیات الصحیة والطبیة الخالصة الموقعب�ة الس�ایتوكینات المنظم�ة ؤدی�ھتدور المھ�م ال�ذي التطورات االخیرة في فھ�م داء الص�دفیةاظھرت ال� العدید من الدراسات قیمت المستویات المصلیة لبعض السایتوكینات االلتھابی�ة االولی�ة .والجھازیة في نشوء المرض مریض�ا ب�داء الص�دفیة 80ض�مت الدراس�ة : داخل الجسم الحي وعالقتھا مع ش�دة الم�رض الم�واد وطرائ�ق العم�ل مجموع��ة داء الص�دفیة الش��دیدة : والثانی�ة ) 30(مجموع�ة داء الص��دفیة الخفیف�ة : مجم��وعتین األول�ى قس�موا عل�ى تراكی�ز ك��ال م��ن انترل��وكین قیس��ت.ف��ردا م��ن األص��حاء مجموع�ة س��یطرة ) 30(قورن�ت نت��ائج البح��ث بــ�ـ ) 50( ئج الدراس�ة اختالف�ات معنوی�ة ف�ي اظھ�رت نت�ا: االس�تنتاجات .السادس والثامن ف�ي مص�ول المرض�ى واالص�حاء ل�دى ) م�ل/بیك�وغرام 17.579( 8-وانترل�وكین) م�ل/بیك�وغرام 32.004( 6-المستویات المصلیة لكال من انترلوكین كم�ا اظھ�رت الدراس�ة ;عل�ى الت�والي) م�ل/بیكوغرام 8.860و 12.640(جمیع المرضى الصدفیة مقارنة باألصحاء بین�ت مجموع�ة داء الص��دفیة إذترلوكین�ات عن�د مقارنتھ�ا بش��دة الم�رض ،ق�ات معنوی�ة ف�ي مس��تویات االنوج�ود فرو ً الش�دیدة فروق� معنوی��ة ف�ي التراكی�ز المص��لیة لك�ال الس�ایتوكینین عن��د مقارنتھ�ا م�ع مجموع��ة داء الص�دفیة الخفیف��ة ا مرض��ى ب��ین عین��اتِ 8-، وانترل��وكین 6-ذل��ك، ك��ان ھن��اك إرتب��اطُ إیج��ابُي ب��ین مس��تویات انترل��وكین فض�الً ع��ن .الصدفیة وتلك المقاییسِ ِمن مستویات السایتوكینات المصلیةِ وھذه قَْد تكُون مؤشرات موضوعیةَ لشدَّةِ المرضَ IHJPAS