简介：AbstractBackground:Degree of mucosal recovery is an important indicator for evaluating the therapeutic effects of drugs in treatment of inflammatory bowel disease (IBD). Increasing evidences has proved that tight junction (TJ) barrier dysfunction is one of the pathological mechanisms of IBD. The aim of this study was to observe whether enhancement of TJ can decrease colitis recurrence.Methods:Eighty C57BL/6 mice were randomly divided into four groups including normal group, colitis group, sulfasalazine (SASP) treated group, and traditional Chinese drug salvianolic acid B (Sal B) treated group. Colitis was established in mice by free drinking water containing dextran sulfate sodium, after treatments by SASP and Sal B, recombinant human interleukin-1β (IL-1β) was injected intraperitoneally to induce colitis recurrence.Results:Compared with sham control, cell apoptosis in colitis group was increased from 100.85 ± 3.46% to 162.89 ± 11.45% (P = 0.0038), and TJ dysfunction marker myosin light chain kinase (MLCK) was also significantly increased from 99.70 ± 9.29% to 296.23 ± 30.78% (P = 0.0025). The increased cell apoptosis was reversed by both SASP (125.99 ± 8.45% vs. 162.89 ± 11.45%, P = 0.0059) and Sal B (104.27 ± 6.09% vs. 162.89 ± 11.45%, P = 0.0044). High MLCK expression in colitis group was reversed by Sal B (182.44 ± 89.42% vs. 296.23 ± 30.78%, P = 0.0028) but not influenced by SASP (285.23 ± 41.04% vs. 296.23 ± 30.78%, P > 0.05). The recurrence rate induced by recombinant human IL-1β in Sal B-treated group was significantly lower than that in SASP-treated group.Conclusions:These results suggested a link between intestinal mucosal barrier dysfunction, especially TJ barrier dysfunction, and colitis recurrence. The TJ barrier dysfunction in remission stage of colitis increased the colitis recurrence. This study might provide potential treatment strategies for IBD recurrence.

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简介：尽管为有类型1糖尿病的个人的小岛移植被显示了产出优异的血葡萄糖控制，它为长期的控制仍然保持不适当。这是部分，由于小岛损害和压力，那能导致贝它房间损失。过量IL-1β的抑制；活动可能最小化小岛损害，因此保存工作。IL-1受体对手(IL-1Ra)，IL-1β的一个内长的禁止者；，保护小岛免受导致cytokine的坏死和apoptosis的伤害。因此，在IL-1β之间的不平衡；并且IL-1Ra可能影响到小岛的allogeneic和自体免疫的回答的功课。我们的组以前证明传播丝氨酸朊酶禁止者人alpha-1-antitrypsin(hAAT)，以及immunomodulatory活动。在现在的学习，我们寻求了决定是否胰腺的小岛hAAT的allograft保护的活动被IL-1Ra调停感应。我们的结果证明hAAT在刺激巨噬细胞在IL-1Ra表示导致了2.04褶层增加并且hAAT-pre-treated小岛接枝在IL-1Ra抄本层次展出了4.851褶层增加，它与中等煽动性的侧面被联系。出人意料地，从IL-1Ra-knockout鼠标被孤立并且在grafting前与hAAT预先对待进野类型的鼠标的小岛在大概从渗入主机房间被导出的intragraftIL-1Ra表示产出增加，当主机的hAAT处理不在时的虽然。确实，hAAT-pre-treated小岛产生了能在有教养的巨噬细胞导致IL-1Ra生产的hAAT免费的调节媒介。最后，我们证明hAAT为p65支持了不同phosphorylation和原子translocation模式，为IL-1Ra要求的一个关键抄写因素表示。

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简介：在过去的十年‘的观点；inflammation’；在皮肤之红色(红色)的原来的特点以外被扩大了，calor(热)，肿瘤(胀大)并且忧伤(疼痛)由Celsus描述了。我们获得了细胞的播放器的更多的详细理解和现在正在被用于并且延长象癌症，肥胖，心疾病，新陈代谢，汽车煽动性的混乱，autoimmunity和传染疾病那样的生物医学的研究的区域的发炎的分子的调停人。天生的cytokines经常是煽动性的回答的中央部件。这里，我们讨论怎么类型我干扰素和interleukin-1cytokine小径代表煽动性的回答的不同、专业化的范畴并且这些怎么互相给发炎柜台调整的调停人调音。

简介：多功能的cytokineinterleukin-1(IL-1)的生物活动被它的受体调停。这研究的目的是决定一个协会是否在1和2受体基因(IL1R1和IL1R2)和表示在mononuclear房间的subpopulations或可溶的IL-1受体的浆液层次上膜界限IL1Rs铺平的IL-1类型在单个核苷酸多型性(SNP)之间存在。这被观察有在SNPrs2234650的遗传型TT的健康个人:C>；T有在他们的表面上表示IL1R1的未经触动的CD14+单核白血球的一个更低的百分比。SNPrs4141134:T>；在IL1R2的C也与表示IL1R2的未经触动的CD3+T房间的百分比被联系了。而且，带SNPrs4141134的CC等位基因的个人:T>；C和SNPrs2071008的TT等位基因:T>；在IL1R2的G在刺激的lipopolysaccharide(LPS)在CD14+单核白血球的表面上有IL1R2s的更低的密度PBMC文化。在摘要，这研究证明IL-1受体基因多型性能是在免疫能力的房间上影响膜界限IL-1受体(IL1R)的表示的因素之一。

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简介：在发炎和白血球过多症之间的潜在的交叉连接有一段时间被讨论了，但是支持这教义的试验性的证据是少见的。特别地，由煽动性的调停人理解为proto-oncogenic生长因素表情的潜在的upregulation负责的机制是重要的。这里，我们调查了高度煽动性的cytokineinterleukin-1贝它的能力(IL-1β；)到导致干细胞因素(SCF)的生产，它是在造血的myeloid细胞的恶意的转变之上控制尖锐myeloid白血球过多症的前进的一个主要造血的生长因素。我们发现了那人的IL-1β；在MCF-7人的上皮的乳癌房间和那导致了SCF的表示/分泌物这个过程取决于组织缺氧可诱导的因素1(HIF-1)抄写建筑群。我们也表明了phosphatidylinositol-3kinase(PI-3K)的一个关键角色rapamycin(mTOR)的/mammalian目标在IL-1β的小径；导致的HIF-1α；在MCF-7房间的累积。重要地，mTOR也被发现在IL-1β起一个作用；导致的SCF生产。而且，为IL-1β的积极关联的一个趋势；并且在健康人的施主的血浆的SCF层次被观察。总的来说，我们的结果表明那IL-1β；，它通常衔接天生、适应的免疫，通过PI-3K/mTOR小径和HIF-1抄写建筑群导致主要haematopoietic/proleukaemic生长因素SCF的生产。这些调查结果强烈支持在发炎和尖锐myeloid白血球过多症之间的串音。

简介：Objective:　Tocomparethedynamicchangesofinterleukin-1(IL-1),interleukin-6(IL-6),andtumornecrosisfactor(TNF)inintermingledskingraftwiththoseinothertypesofskingraftsinrats.　　Methods:　A10%-15%third-degreeburnwascreatedin180Spregue-Dawley(SD)rats.Afterremovingthescar,skingraftswereperformedontheopenwoundsimmediatelywithautoskin(aus,n=54),alloskin(als,n=54)andintermingledskin(n=36).Thatistosay,intheintermingledskingraft,abigpieceofalloskin(mals)wasgraftedfirst,and3dayslater,smallpiecesofautoskin(maus)wereembeddedinthealloskin.Therest36ratsweretakenasthecontrols.AndthebiologicalactivitiesofIL-1,IL-6andTNFingraftsheetsineachgroupweredetectedafterskingraft.　　Results:　ThelevelsofIL-1,IL-6andTNFintheausgroupdecreasedsteadilyaftertheirinitialelevations,whereasinthealsgrouptheyincreasedsignificantlyandkeptonthepeaklevelinthelaterphases.Intheintermingledgroup,thereappearedalowestIL-1levelinthemalsandahighestoneinthemaussimultaneouslyat7(4)days(Thenumberoutofparenthesisisthedaysaftertransplantingwithalloskinsheets,andthenumberinparenthesisisthedaysafterembeddingautoskinsheetsintheintermingledskingraft.Similarlyhereinafter.)afterskingraft(P<0.01),andthehighlevelinthemausabruptlydecreasedat14(11)daysafterskingraft.Atexactlythesamephaseonday7(4),aprominentpeakedIL-6inthemalsoccurred.Inthelaterphases,thelevelsofTNFremainedrelativelylowbothinthemalsandinthemaus.Fromday7(4)on,eachcytokinefluctuationinthemalssynchronizedwiththatinthemaus.Thelongertheposttransplantationperiodlasted,themorethepositivecytokinecorrelatedbetweenthemalsandthemaus.　　Conclusions:　ThelowlevelsofIL-1andTNFmaybeimportantfactorstolightentheintensityoflocalrejectionintheintermingledskingraft.Thetempo

简介：Objective:Tostudythecellularimmunitystatusofpatientswithrecurrentgenitalherpes.Methods:Serumlevelsofinterlukin-2anditssolublereceptorandinterlukin-6weremeasuredbyELISAin34patientswithrecurrentgenitalherpes.Results:SerumlevelsofIL-2andIL-6weresignificantlydecreasedinpatientscomparedtohealthycontrols(P<0.01),andthelevelofsIL-2Rwassignificantlyincreasedinpatientswithrecurrentgenitalherpes(P<0.01).Therewerenosignificantdifferencesinallvariablesamongstpatientsregardingrelapsestageandremissionstage(P>0.05).Conclusion:Therewasacellularimmunedeficiencyinpatientswithrecurrentgenitalherpes.

简介：TheinvivoeffectsofPhytolaccaacinosapoly-saccharidesI(PEP-I)onimmunologiccytotoxicityofmouseperitonealmacrophagesanditsproductionoftumornecrosisfactor(TNF)andinterleukin1(IL-1)werestudied.PEP-I80or160mgkgwasgiveniptwiceevery4day.BothdoseswerefoundtohavesignificantenhancingactivityonmacrophagescytotoxicityagainstS180sarcomacellsandmalignanttransformedfibroblastL929cells.PeritonealactivatedmacrophageswereincubatedwithLPSfor2and24hrstoinduceTNFandIL-1,respectively.TheTNFandIL-1activitiesweretestedfromcytotoxicityagainstL929cellsinanabsorbenceassayofenzymaticreactionandproliferationofthymocytesco-stimulatedassayseparately.TheoptimaltimeforTNFproductionwasfoundonday8.SignificantincreasesinTNFandIL-1wereobserved.IncomparisonoftheeffectofPEP-IonTNFwiththatofknownprimingagentBCG,therewasnodifferencebetweenthem,butPEP-IhadahigheffectonIL-1.Theseresultssug

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简介：Interleukin-18(IL-18)wasdiscoveredasaninterferon-γ-inducingfactorandhadacriticalroleininflammatoryandimmuneresponse.Itstimulatesnaturalkiller(NK)andTcellsandenhancesTh1immuneresponse.Theseactivatedimmunecellseliminatecancercellsandvirus-infectedcellseffectively.However,IL-18hasalsobeenfoundtopromotetumorprogression.HigherexpressionorsecretionlevelofIL-18isdetectedinvariouscancercellsincomparisonwithnormalcontrol,andIL-18isabletoinduceangiogenesis,migration/metastasis,proliferationandimmuneescape.ThesedualeffectsandthemechanismofIL-18needtobeinvestigatedfurtherasitrelatestocancer.

简介：Demyelinationofthecentralnervoussystem(CNS)isahallmarkofmultiplesclerosis(MS),chronicinflammatoryandneurodegenerativedisease.Chronicdemyelinationfavorsneurodegenerationofdenudedaxons,whichisamajorcauseofirreversibleneuronaldeficitsanddisabilityinMSpatients(Lucchinettietal.,2000).MSremainsanincurabledisease,despiteformida-

简介：Objective:Toinvestigatetherolesofinterleukin-2(IL-2)andinterleukin-10(IL-10)inpathogenesisofearlysyphilis.Methods:TheserumlevelsofIL-2andIL-10in48patientswithearlysyphilisweredetectedbyABC-ELISA.Results:(1)ThelevelofIL-2inthepatientswithearlysyphiliswassignificantlyhigherthanthatinhealthycontrols,whilethatofIL-10waslower(P<0.001andP<0.001).(2)ThelevelsofIL-2andIL-10werealmostidenticalinpatientswithprimaryandsecondarysyphilis(P>0.05),aswellasbetweendif-ferentRPRtiters(P>0.05).(3)Aftertherapy,thelevelofIL-2decreasedmarkedly(P<0.05),whilethatofIL-10increase(p>0.05).(4)AsignificantcorrelationwasfoundbetweentheserumlevelsofIL-2andIL-10(r=0.5385P<0.05).Conclusions:Th1up-regulationoccursinpatientswithearlysyphilis,andplaysanactiveroleinfightingagainstTPinfection.

简介：AlthoughithasbeenknownthatγδTcellsmayplayanimportantroleintheimmuneresponsetoinfectionofMycobacteriumtuberculosis(M.tb),themechanismsbywhichtheγδTcellsparticipateintheinnateand/oracquiredimmunitytotuberculosis(TB)havenotbeenfullelucidated.Inthepresentstudy,27patientswithactivepulmonaryTBand16healthydonors(HD)wereperformed.WefoundthatproportionofIL-17-producingcellsamonglymphocytewassimilarbetweenTBpatientsandHD,whereastheproportionsofγδTcellsinIL-17-producingcells(59.2%)andIL-17-producingcellsinγδTcells(19.4%)inperipheralbloodweremarkedlyincreasedinTBpatientswhencomparedtothoseinHD(43.9%and7.7%,respectively).Inaddition,theproportionsofIFN-γ-producingγδTcellsinTBpatientswereobviouslylowerthanthatinHD.Uponre-stimulatedwithM.tbheat-treatedantigen(M.tb-HAg)invitro,fewerIL-17-producingγδTcellsweregeneratedfromHDandTBpatients,whereasIFN-γ-producingγδTcellswereincreasedinTBpatientscomparedtothatinHD.OurfindingsinTBpatientsandhealthyhumanwereconsistentwithothermurineinvestigationthattheIL-17-producingγδTcellsweremainsourceofIL-17inmousemodelofBCGinfection,suggestingthatγδTcellsmightbeinvolvedintheformationoftuberculargranulomainpulmonaryTBpatients,butneedfurtheridentification.

简介：AbstractBackground:Interleukin-18 (IL18) gene polymorphisms are related to many inflammatory and autoimmune diseases. However, a correlation analysis between IL18-607C/A and -137G/C gene polymorphisms and Takayasu arteritis (TA) is lacking.Methods:This study enrolled 200 patients with TA as the case group and 334 region-, age-, and sex-matched healthy subjects as the control group. We genotyped alleles and genotypes at positions -607 and -137 of the IL18 gene and analyzed the distribution frequencies. Mann-Whitney U test, t test, Chi-squared test and Hardy-Weinberg equilibrium were performed.Results:After adjusting for risk factors, the adjusted odds ratios and 95% confidence intervals at position -607C/A were 0.533, 0.391 to 0.880 (P = 0.010); 0.266, 0.586 to 1.002 (P = 0.051); and 0.122, 0.552 to 1.420 (P = 0.613) under the dominant, additive, and recessive models, respectively. For the -137G/C polymorphism, the adjusted odds ratios and 95% confidence intervals were 1.571, 1.068 to 2.311 (P = 0.022); 1.467, 1.086 to 1.980 (P = 0.012); and 1.815, 0.901 to 3.656 (P = 0.095) under the dominant, additive, and recessive models, respectively. Moreover, regardless of the model used, we found no statistical difference in distribution frequency between the active and quiescent states of TA for the -607C/A (P = 0.355, 0.631, and 0.705, respectively) and -137G/C polymorphisms (P = 0.205, 0.385, and 0.208, respectively).Conclusions:The IL18-607C/A gene polymorphism may decrease the risk of TA, and thus is a protective factor, whereas -137G/C may increase the risk of TA, and thus is a risk factor. However, neither polymorphism was related to activity (active vs. quiescent) of TA.

简介：Theaimofthisstudyistoinvestigatewhetherthreemononucleotidepolymorphismsatthelocus-1082,-819and-592inthepromoterregionoftheIL-10geneareassociatedwithchronicseverehepatitis.TheIL-10-592andIL-10-1082polymorphismsweregenotypedbypolymerasechainreaction-restrictionfragmentlengthpolymorphismanalysis(PCR-RFLP)whilepolymerasechainreaction-se-quencespecificprimer(PCR-SSP)assaywasusedtotesttheIL-10-819polymorphism.Thepolymor-phismsofIL-10-1082,-819and-592genesweredetectedin98patientswithchronicseverehepatitis(CSH),478patientswithchronichepatitisB(CHB),223asymptomatic(chronic)HBVcarriers(ASC)and267patientswithself-restrictedHBV.Therewassignificantdifferenceofthepolymor-phismsofIL-10-1082,IL-10-819andIL-10-592genesbetweenCSHgroupandothergroups.Thefre-quencyofAAgenotypeatIL-10genepromoter-1082locusinchronicseverehepatitispatientswashigherthanthatinasymptomaticHBVcarriers(X~2=13.314,P=0.001),andself-restrictedHBVpatients(X~2=13.545,P=0.000);thefrequencyofCCandACgenotypeatIL-10genepromoter-592locusinchronicseverehepatitispatientswashigherthanthatinchronichepatitispatients(X~2=15.970,P=0.000)(X~2=20.414,P=0.000),asymptomaticHBVcarriers(X~2=21.283,P=0.000)(X~2=28.309,P=0.000)andself-restrictedHBVpatients(X~2=17.047,P=0.000)(X~2=16.528,P=0.000);thefrequencyofTCgenotypeatIL-10genepromoter-819locusinchronicseverehepatitispatientswashigherthanthatinchronichepatitispatients(X~2=58.961,P=0.000),asymptomaticHBVcarriers(X~2=53.255,P=0.001)andself-restrictedHBVpatients(X~2=39.616,P=0.001).Sointerleukine-10genepolymorphismwasassociatedwiththechronicsevereheoatitis.

简介：可移植的试验性的肿瘤模型被构造对肿瘤复发和转移学习recombinant人interleukin-15(rhIL-15)的活动。结果证明那肿瘤小瘤形成被延迟，肿瘤生长与rhIL-15在处理以后在LA795肺腺癌的下的肿瘤模型被禁止，并且与rhIL-15对待的T739忍受肿瘤的老鼠的幸存率比与盐的任何一个或与rhIL-2的一样的剂量对待的老鼠的高得多。这indicats那rhIL-15antitumor最好在一样的剂量水平比rhIL-2完成。在一些，rhIL-15对待老鼠，皮下地接种的肿瘤房间被根除，没有肿瘤形成甚至在肿瘤以后的138天房间接种。没有肿瘤的老鼠与实时肿瘤房间被重新质问，没有肿瘤这些老鼠在所有在下列二个月内重新发生，显示全身的免疫开发了的那长持续的antitumor。肿瘤复发和转移与rhIL-15，然而并非与rhIL-2的一样的剂量在处理以后显著地被禁止，这也被显示出，在LA795肺腺癌的皮下地并且静脉内地传播的肿瘤模型。同时，splenocytes的CTL和NK房间活动从与任何一个rhIL-15被对待的忍受肿瘤的老鼠获得了或rhIL-2是显著地提高的两个。然而，CTL和NK房间活动的改进在rhIL-15是更重要的在rhIL-2比那对待老鼠对待的老鼠。这建议在vivo的rhIL-15的反肿瘤效果被在肿瘤免疫者反应提高CTL和NK房间活动完成。细胞与分子的免疫学。2008；5(3):189-196。