Expression Of IL-18IL-33and IL-35in The Serum Of Patients With Allergic Purpura

Objective：Allergic purpura (Henoch—schonlein purpura，HSP）is ahypersensitivity vasculitis,damages the capillaries and postcapillary venule ofthe skin or other organs.Mainly involving the skin, gastrointestinal system andkindney,with or without pain of joints or arthritis.Children are high-riskgroups and the condition easy recurrent. At present,t he pathogenesis ofallergic purpura has not been fully clear,more resercher thought it is concernedwith T cell subgroup，helper T lymphocyte (Th1/Th2) immune responseimbalances and Th17, Treg cell imbalances.Interleukin18(IL-18) is a complex pro-inflammatory cytokines,play atwo-way role in the inflammatory. It can not only pormote the Th1typeimmune response, under certain conditions,also can promote the Th2typeimmune response. IL-18belongs to IL-1family, is one of the importantregulatory factor of congenital and adaptive immune responses. It expressed inmany cells such as lymphocytes and activation macrophages etc. To activate Tcells and macrophages, produce a series of cytokines. Promote thedevelopment of inflammation. IL-18plays an important role in the regulatingthe inflammatory response and the immune response. Interleukin-33(IL-33) isfound by Schmitz in2005. The study found that IL-33belongs to IL-1familyof cytokines and mainly secreted by activated T cells. It participates inimmunoregulation and inflammation.The structure of IL-33and IL-18mostsimilar.It participate in the inflammatory process of Th2cells involved,adjustthe Th2cytokines activation by the signal pathway mediates the biologicalactivities.Interleukin-35(IL-35) belongs to a type Ⅰ cytokine superfamilymember. It is a new member in the IL-12family. Collison preliminaryconfirmed IL-35is mainly secreted by Treg cells and take some negativeeffects on the immune response. IL-35can inhibit inflammation and prevent excessive immune reaction. So far, according to a study by IL-35caneffectively enhance the function of Treg subsets, and effectively restrain Th17cell proliferation, differentiation.It also inhibits the body’s excessive immuneresponse and prevents inflammation in the body’s immune injury. Expressionlevels of IL-18IL-33and IL-35in the serum of patients with allergic purpurawere detected by double antibody sandwich ELISA assay in the experiment.Explore the role of IL-18IL-33and IL-35in the pathogene of allergicpurpura.A more particular knowledge of the function of proinflammatorycytokine and anti-inflammatory cytokine in pathogenesis of allergic purpura.Methods：Patients with allergic purpura from the dermatology clinic ofthe Second Hospital of Hebei Medical University during January2013to June2013were choosed as the case group. The case group had30cases,14malesand16females, age range8to27years, mean age16.57±4.06years.Selection standard:1Patients with allergic purpura had typical skin lesions（none of stomachache arthrodynia and kidney damage）and the blood plateletcount are normal.2Patients had not hemorrhagic disorders in the family.3They had not received system treatment of glucocorticoids and cytotoxicdrugs which affected the immune function in last four weeks before theexperiment.4None of them had autoimmune diseases or other serious chronicsystemic diseases.Normal control group came from healthy hospital care staff.The case group had20cases,9males and11females, age range12to28years,mean age18.05±3.59years.Through t-test, the sex and age had no significantdifference with the case group. Adopted vein venous blood2ml from casegroup and normal control group into tubes, centrifuged to collect serumsamples and saved at-70°C refrigerator. Finnaly detected expression ofIL-18、IL-33and IL-35in the surem by double antibody sandwich ELISA test.Applicated SPSS13.0software for statistical analysis, datas of case group andcontrol group showed normal distribution by normality test, so we used twoindependent sample t test to analyze whether the difference between casegroup and control group IL-18IL-33and IL-35in the serum had significantdifference or not. P <0.05had statistically significance. Result:1The expression level of IL-18in serum of case group142.41±92.06washigher than that of normal control group78.89±21.58, the difference wasstatistically significant (t=3.63P=0.001P<0.05).2The expression level of IL-33in serum of case group65.26±33.30washigher than that of normal control group37.91±30.97, the difference wasstatistically significant (t=2.92P=0.005P<0.05).3The expression level of IL-35in serum of case group58.55±16.32waslower than that of normal control group81.03±29.90, the difference wasstatistically significant (t=-3.07P=0.005P<0.05).Conclusion:1The expression level of IL-18in serum of case group was higher thanthat of normal control group,the difference was statistically significant.Sugge-stting that IL-18may participate in the early stage inflammation of allergicpurpura.2The expression level of IL-33in serum of case group was higher thanthat of normal control group,the difference was statistically significant.Indicating that IL-33could be play some role in the pathogenesis of allergicpurpura. Due to the structure of IL-33and IL-18most similar,IL-33may takesome similar efforts with IL-18.Meanwhile, it indirectly reflected the functionof Th1/Th2cells in allergic purpura.3The expression level of IL-35in serum of case group was lower thanthat of normal control group, the difference was statistically significant.Indicating that the level of IL-35was inhibited in the early inflammation ofallergic purpura, so the protect function also recede.According to thecharacteristic of IL-35, presumably,I L-35could be play an anti-inflammationrole.It is a protection factor.