阿托伐他汀对动脉粥样硬化兔肿瘤坏死因子α和组织因子水平的影响

目的 研究阿托伐他汀对动脉粥样硬化兔血浆和外周血单核细胞表达肿瘤坏死因子α和组织因子水平的影响.方法 采用高胆固醇饮食法建立动脉粥样硬化兔模型(n=12),随机给予阿托伐他汀或淀粉4周,同时6只兔以普通饲料喂养.12周后,取各组兔主动脉测定斑块内膜面积,分离外周血单核细胞培养24 h.采用酶联免疫吸附法检测血浆和细胞培养上清液中肿瘤坏死因子α及细胞膜组织因子水平.结果 阿托伐他汀能降低主动脉斑块面积百分数、血浆和外周血单核细胞肿瘤坏死因子α及组织因子水平(均P<0.01);主动脉斑块面积百分数、血浆及外周血单核细胞肿瘤坏死因子α和组织因子水平两两之间呈正相关(均P<0.01).结论 阿托伐他汀在降低胆固醇同时,还可通过降低肿瘤坏死因子α和组织因子水平发挥抗动脉粥样硬化作用.     

阿托伐他汀对慢性心力衰竭患者心功能及肿瘤坏死因子-α的影响

目的:探讨阿托伐他汀对慢性心力衰竭患者左室射血分数(LVEF),脑利钠肽(BNP)及肿瘤坏死因子(TNF-α)、核转录因子(NF-κB)活性的影响。方法:将血脂正常的慢性心力衰竭患者50例随机分为对照组(25例)和他汀组(25例)。两组均接受常规治疗(利尿剂、ACEI、或洋地黄、β-受体阻滞剂),他汀组再加用阿托伐他汀(20mg/d)治疗,治疗前及治疗后12周均测LVEF、血清BNP、TNF-α、外周血单个核细胞NF-κB活性。结果:BNP、TNF-α、NF-κB活性与心力衰竭严重程度正相关,治疗12周后,两组TNF-α、BNP、NF-κB活性均下降(P<0.05),LVEF升高(P<0.05),且以他汀组变化更明显,与对照组比较差异有统计学意义(P<0.05)。结论:慢性心力衰竭患者在接受常规治疗的同时,加用阿托伐他汀治疗可明显改善LVEF、降低BNP、TNF-α及NF-κB活性。     

罗格列酮联合阿托伐他汀对单核细胞分泌肿瘤坏死因子α的影响

目的 研究罗格列酮联合阿托伐他汀干预对无糖尿病的急性冠脉综合征（ACS）患者外周血单核细胞分泌肿瘤坏死因子α（TNF-α）的影响。方法 分离无糖尿病的ACS患者外周血单核细胞,设置对照组（等容积的二甲基亚砜）、阿托伐他汀（1 μmol/L）组、罗格列酮（1 μmol/L）组及二者联合组（阿托伐他汀1 μmol/L加罗格列酮1 μmol/L组） 4个组,分别与所分离的外周血单核细胞共同孵育24 h后,用夹心酶联免疫吸附测定法检测细胞培养上清液TNF-α,用逆转录聚合酶链反应（RT-PCR）测定TNF-α mRNA的表达。结果 与对照组相比较,阿托伐他汀组、罗格列酮组及联合组对无糖尿病ACS患者外周血单核细胞分泌TNF-α［分别为(229±24)ng/L、(236±28)ng/L、(159±29)ng/L vs (306±40)ng/L,均P<0.05］及TNF-α mRNA的相对半定量吸光值（A）比值（分别为0.35±0.12,0.39±0.11,0.26±0.06 vs 0.78±0.14,均P<0.05）均降低,且罗格列酮联合阿托伐他汀组比阿托伐他汀组、罗格列酮组降低更显著（均P<0.05）。结论 阿托伐他汀和罗格列酮都可通过降低无糖尿病的ACS患者外周血单核细胞产生分泌TNF-α,发挥阿托伐他汀和罗格列酮的抗炎作用,且二者联合干预具有协同作用,防治效果更佳。     

阿托伐他汀对慢性心力衰竭病人心功能及肿瘤坏死因子的影响

目的探讨慢性心力衰竭(CHF)病人肿瘤坏死因子(TNF-α)的变化及阿托伐他汀对其的干预作用。方法将70例CHF病人随机分为阿托伐他汀组和常规治疗组,采用放免法测定CHF病人TNF-α浓度、左室射血分数(LVEF)、左室舒张末内径(LVDd)。结果随着NYHA心功能分级的升高,TNF-α逐渐升高(P0.05);TNF-α与LVEF呈负相关,与LVDd呈正相关;阿托伐他汀组治疗后TNF-α水平显著降低(P0.05),LVEF显著提高(P0.05),LVDd显著降低(P0.05),与常规治疗组治疗后比较差异也有统计学意义(P0.05)。结论在常规治疗的基础上加用阿托伐他汀能进一步降低TNF-α水平,改善心功能。     

阿托伐他汀对血脂正常高血压患者血清TNF-α和IL-6的影响

目的：观察阿托伐他汀对血脂正常高血压患者血清肿瘤坏死因子（TNF）-α和白细胞介素（IL）-6的影响。方法：72例血脂正常高血压患者被随机分为常规治疗组（36例,常规降压治疗）与阿托伐他汀组（36例,在常规降压治疗基础上加服阿托伐他汀）,治疗8周。分别于治疗前后检测患者血压及血清TNF-α和IL-6水平。结果：治疗前,两组患者血压及血清TNF-α和IL-6水平比较,差异无显著性（P〉0.05）;治疗后,与常规治疗组比较,阿托伐他汀组患者血压[收缩压（132.45±10.34）mmHg比（128.55±9.22）mmHg,舒张压（88.24±8.66）mmHg比（85.18±8.25）mmHg]及血清TNF-α[（9.43±2.02）ng/L比（7.92±2.13）ng/L]和IL-6[（20.12±3.55）ng/L比（16.65±3.27）ng/L]水平均明显降低（P〈0.05或P〈0.01）。结论：阿托伐他汀对血脂正常高血压患者能协同降压,其机制可能与降低血清肿瘤坏死因子-α和白细胞介素-6水平,抑制炎症反应有关。     

阿托伐他汀对脂肪细胞分泌白细胞介素-6的影响

我们通过建立高胆固醇血症兔模型来观察阿托伐他汀对脂肪细胞分泌白细胞介素 6 (IL 6 )的影响、并进一步探讨其可能机制。一、材料与方法1.动物模型 :14只 3月龄的健康雄性新西兰兔 ,单笼饲养 1周后记录体重并进行基线血脂分析 ,然后随机给 10只兔喂食 1%的高胆固醇饲料 ,4只兔进食普通饲料。第 8周再次测血脂和体重 ,第 9周开始在高胆固醇饮食组随机给予阿托伐他汀 1 5mg·kg-1·d-1(n =5 )或淀粉 1 5mg·kg-1·d-1(n =5 )。 2周后复测血脂及体重 ,取腹股沟处皮下脂肪组织进行脂肪细胞培养。采用Agatha等的方法并作适当修改进行脂肪细胞…     

瘦素对血管内皮细胞肿瘤坏死因子-α表达的影响及阿托伐他汀对其的干预简

目的 探讨瘦素对血管内皮细胞（vascular endothelial cells,VECs）肿瘤坏死因子-α（tumor necrosis factor-α,TNF-α）表达的影响及阿托伐他汀对其的干预作用.方法 采用原代细胞培养方法建立大鼠VECs细胞模型;100 ng/mL瘦素刺激内皮细胞0、1、3、6、12 h;10 μmol/L阿托伐他汀干预细胞0、1、3、6、12、24 h,再用100 ng/mL瘦素干预细胞6h.运用双抗体夹心酶联免疫吸附试验（ELISA）法测定各组细胞上清液TNF-α表达浓度.结果 瘦素刺激组TNF-α表达高于对照组,且随着瘦素作用时间延长,TNF-α表达也随之增加.阿托伐他汀组TNF-α的表达低于对照组,且随着阿托伐他汀作用时间的延长,TNF-α表达也随之降低,24 h抑制作用最明显.结论 瘦素时间依赖性诱导血管内皮细胞TNF-α的表达,阿托伐他汀可以减弱瘦素诱导的TNF-α的表达.     

瑞舒伐他汀对急性冠脉综合征患者血清高敏C反应蛋白和肿瘤坏死因子α的影响

目的通过观察瑞舒伐他汀治疗急性冠脉综合征（ACS）,患者血清高敏C反应蛋白（hs-CRP）和肿瘤坏死因子α（TNF-α）水平变化,探讨瑞舒伐他汀对ACS患者炎症反应的影响。方法选择ACS患者70例及正常对照组30例,ACS患者在常规治疗基础上采用瑞舒伐他汀治疗,比较治疗前后血清hs-CRP和TNF-α的水平变化。结果治疗组ACS患者治疗前血清hs-CRP和TNF-α水平与对照组比较,差异有统计学意义（P〈0.01）;治疗组治疗4周后血清hs-CRP和TNF-α水平均与治疗前比较,差异有统计学意义（P〈0.01）,与对照组比较,差异亦有统计学意义（P〈0.01）;以hs-CRP为应变量,血清hs-CRP与TNF-α呈正相关（r=0.712,P〈0.01）。结论 ACS患者存在着高水平的hs-CRP及TNF-α,经瑞舒伐他汀治疗后血清hs-CRP及TNF-α平显著降低,显示瑞舒伐他汀可降低炎症反应,动态检测血清hs-CRP和TNF-α水平变化可作为ACS发生的预测指标。     

阿托伐他汀对CHF患者血清炎症因子水平的影响及意义

目的探讨阿托伐他汀治疗慢性心力衰竭（CHF）的疗效及机制。方法将60例CHF患者随机分为阿托伐他汀组和常规组,两组均予CHF常规治疗,阿托伐他汀组加用阿托伐他汀,疗程均为4周。治疗前后分别采用免疫透射比浊法和放射免疫分析法检测血清血清C反应蛋白（CRP）、IL-6和TNFα-水平,行心脏超声检查测定左室射血分数（LVEF）;检测结果与30例健康体检者（正常组）比较。结果治疗前所有CHF患者血清CRP、IL-6和TNFα-水平均明显高于正常组（P〈0.05）;治疗后均明显降低（P〈0.05）,但阿托伐他汀组较常规组降低更明显（P〈0.05）。与常规组比较阿托伐他汀组LVEF升高更明显（P〈0.05）。结论阿托伐他汀治疗CHF短期效果确切,其机制可能为降低血清炎症因子水平。     

不同剂量阿托伐他汀对急性脑梗死患者高敏C反应蛋白、白细胞介素6、肿瘤坏死因子α的影响

目的 探讨不同剂量阿托伐他汀对急性脑梗死患者高敏C反应蛋白（hs-CRP）、白细胞介素6（IL-6）及肿瘤坏死因子α（TNF-α）水平的影响.方法 选择84例急性脑梗死患者分为两组（A组和B组）,在常规治疗的基础上,A组口服阿托伐他汀10 mg/d,B组采用口服阿托伐他汀20 mg/d,两组均治疗4周,观察两组患者用药前后hs-CRP、IL-6及TNF-α的变化.结果 阿托伐他汀可降低急性脑梗死患者血清hs-CRP、IL-6及TNF-a水平,并呈量效关系.结论 大剂量应用阿托伐他汀可明显减轻急性脑梗死炎性反应.     

重症狼疮肾炎患者血清TNF-α与sTNF-R水平及甲泼尼龙与环磷酰胺双冲击治疗对其的影响

目的探讨重症狼疮肾炎(SLN)患者血清肿瘤坏死因子!(TNF-!)、可溶性肿瘤坏死因子受体(sTNF-R)的水平、sTNF-R/TNF-!比值及甲泼尼龙(MP)与环磷酰胺(CTX)双冲击治疗对其的影响。方法采用双抗体夹心酶联免疫吸附试验(ELISA)检测35名健康人(正常对照组)和38例SLN患者经MP与CTX双冲击治疗前后血清TNF-!、sTNF-RⅠ、sTNF-RⅡ的水平;抗双链DNA抗体采用ELISA法测定;抗核抗体采用间接免疫荧光法检测;补体C3、C4含量采用速率散射比浊法测定。结果SLN患者血清中TNF-!、sTNF-RⅠ、sTNF-RⅡ水平及TNF-!/sTNF-RⅠ、TNF-!/sTNF-RⅡ比值均显著高于正常对照组(P<0.01),且sTNF-RⅡ增高幅度明显高于sTNF-RⅠ(P<0.01),TNF-!、sTNF-RⅠ、sTNF-RⅡ水平与系统性红斑狼疮疾病活动指数(SLEDAI)评分、抗核抗体、抗双链DNA抗体、血沉、24h尿蛋白定量、血尿素氮(BUN)、血肌酐(Scr)呈显著正相关(P<0.05或P<0.01),与补体C3、C4、内生肌酐清除率(Ccr)呈显著负相关(P<0.05或P<0.01);sTNF-RⅠ与sTNF-RⅡ之间呈显著正相关(P<0.01)。MP与CTX双冲击治疗能显著降低SLN患者血清TNF-!、sTNF-RⅠ、sTNF-RⅡ水平及sTNF-RⅠ/TNF-!、sTNF-RⅡ/TNF-!比值(P<0.01)。结论TNF-!、sTNF-R参与了SLN的发病过程,血清TNF-!、sTNF-RⅠ、sTNF-RⅡ在一定程度上可反映SLN患者肾脏损害程度、病情轻重。动态观察血清TNF-!、sTNF-RⅠ、sTNF-RⅡ水平及sTNF-R/TNF-!比值,有助于判断SLN的狼疮活动、治疗效果及预后。MP与CTX双冲击疗法可能通过抑制SLN患者单核/巨噬细胞、T细胞产生TNF-!而发挥治疗作用。     

阿托伐他汀对高胆固醇血症兔脂肪细胞分泌白介素-6的影响

目的 探讨阿托伐他汀对高胆固醇血症兔脂肪细胞分泌白介素-6(IL-6)的作用及其机制。方法 选取健康雄性新西兰兔14只,随机分为正常饮食组、高胆固醇血症阿托伐他汀组和淀粉组,取皮下组织进行脂肪细胞培养,并行各组兔主动脉动脉粥样硬化病变面积测定,采用酶联免疫吸附测定法检测血浆和脂肪细胞培养上清液中IL-6的水平。并检测脂肪细胞过氧化物酶增殖体激活型受体(PRAR)γ mRNA的表达。结果 阿托伐他汀组与淀粉组比较,动脉粥样硬化病变的面积显著降低36％,与血浆IL-6的水平显著相关(r=0.906,P<0.01)。血浆IL-6的水平与脂肪细胞培养上清液中IL-6水平相关(r=0.849,P<0.01)。脂肪细胞培养上清液中IL-6水平与PPARγmRNA的表达呈负相关(r=-0.900,P<0.01)。结论 阿托伐他汀可降低高胆固醇血症兔血浆中IL-6水平,并可通过增加脂肪细胞PPARγmRNA的表达来抑制其分泌IL-6。     

慢性阻塞性肺疾病大鼠模型肿瘤坏死因子α及受体的表达及意义

目的探讨肿瘤坏死因子α（TNF—α）与肿瘤坏死因子受体1（TNFR1）在慢性阻塞性肺疾病（COPD）发生发展中的意义。方法建立吸烟大鼠COPD模型,测定大鼠的肺功能及其血清和BALF的细胞数,观察肺组织病理形态变化和肺平均内衬间隔（MLI）和平均肺泡数（MAN）评估肺气肿的程度。用酶联免疫吸附测定（ELISA）法检测大鼠血清和支气管肺泡灌洗液（BALF）中TNF—α及TNFRI的表达。结果COPD组BALF中白细胞、中性粒细胞及巨噬细胞数增高。COPD组肺功能指标FEV0．3、FEV0．3／FVC％和PEF分别为（1．86±0．22）ml、（65．064-8．40）％、（18．84±1．56）ml/s,比正常组（4．20±0．25）ml、（85．56±5．85）％、（47．24±7．28）ml／s下降。COPD组MLI、MAN分别为（77．32±28．73）um／个、（232．00±97．18）个／mm。而正常组为（43．96±7．16）um／个、（392．84±24．41）个／mm^2,COPD组MLI增加而MAN减少;COPD组血清和BALF的TNF—α、TN—FRl表达增高,分别为TNF—α（117．98±33．82）pg／ml、（155．10±27．60）pg／ml而TNFR1为（85．00±16．34）pg／ml、（98．13±11．97）pg／ml而正常组为TNF-α（73．98±16．41）ps／ml、（79．20±27．70）ps／ml,TNFR1为（58．82±24．57）pg／ml、（61．89±26．25）pg／ml。COPD组BALF的TNFR1表达与MLI呈正相关（r=0．79,P=0．004）与MAN呈负相关（r=-0．626,P=0．039）。两组间不比较均有统计学差异（P〈0．05）。结论TNF—α、TNFR1作为炎症介质在COPD的发生、发展中起重要促进作用。     

Epigenetic modifications of tumor necrosis factor-alpha in joint cartilage tissue from osteoarthritis patients - CONSORT

Background:Osteoarthritis (OA) remains one of the most common osteopathy for centuries, which can be attributed to multiple risk factors including mechanical and biochemical ones. More and more studies verified that inflammatory cytokines play important roles in the progression of OA, such as tumor necrosis factor-alpha (TNF-α). In this study, we aimed to investigate the relationship between epigenetic manifestations of TNF-? and the pathogenesis of OA.Methods:Totally, 37 OA patients’ cartilage was collected through the knee joint and 13 samples of articular cartilage as healthy control was collected through traumatic amputation. Real-time PCR, Western blot and ELISA analysis were performed to observe the expression of target genes and proteins in collected samples.Results:Compared with the healthy control group, TNF-? was over-expressing in cartilage which was collected from OA patients. DNA hypomethylation, histone hyperacetylation and histone methylation were observed in the TNF-? promoter in OA compared with normal patients, and we also studied series of enzymes associated with epigenetics. The results showed that by increasing DNA methylation and decreasing histone acetylation in the TNF-? promoter, and TNF-? over-expression in OA cartilage was suppressed, histone methylation has no significant correlation with OA.Conclusion:In conclusion, the changes of epigenetic status regulate TNF-α expression in the cells, which are pivotal to the OA disease process. These results may give us a better understanding of OA and may provide new therapeutic options.     

Genetic polymorphisms of adiponectin and tumor necrosis factor-alpha and nonalcoholic fatty liver disease in Chinese people

Background and Aim:  Hypoadiponectinemia and high tumor necrosis factor-alpha (TNF-α) levels are associated with the development of nonalcoholic fatty liver disease (NAFLD). This study aimed to investigate the genetic polymorphisms of adiponectin and TNF-α in Chinese NAFLD patients and their association with disease severity.
Methods:  Seventy-nine patients with histology-proven NAFLD (61 with simple steatosis and 18 with stage 2–4 fibrosis) and 40 controls were tested for the nucleotide polymorphisms at adiponectin −11 391, −11 377, +45, and +276 and TNF-α promoters −863, −308, and −238.
Results:  There was no significant deviation in the adiponectin and TNF-α gene polymorphisms between NAFLD patients and controls, or between patients with simple steatosis and those with stage 2–4 fibrosis. NAFLD patients with −11377G and +45G at the adiponectin gene were more likely to have hypertriglyceridemia. On multivariate analysis, older age, higher body mass index, and higher fasting glucose were independent factors associated with stage 2–4 fibrosis in NAFLD patients.
Conclusions:  Adiponectin and TNF-α gene polymorphisms were not shown to be associated with NAFLD or significant fibrosis in Chinese people. The adiponectin −11377G and +45G alleles were associated with hypertriglyceridemia in NAFLD patients. Since the current study is not adequately powered to detect smaller differences in allele frequencies, larger-sized studies in different ethnic groups are required.     

肥胖及2型糖尿病患者血清视黄醇结合蛋白4、脂联素与肿瘤坏死因子α水平变化及其相关性研究

目的：检测肥胖及2型糖尿病患者血清视黄醇结合蛋白（RBP4）、脂联素及肿瘤坏死因子α（TNF-α）水平变化,探讨三者的相关性。方法选择135例上海地区中国人,分为正常糖调节正常体质量（NBM-NGR）组、正常糖调节超重/肥胖（OW/OB-NGR）组、2型糖尿病正常体质量（NBM-T2DM）组及2型糖尿病伴超重/肥胖（OW/OB-T2DM）组,测定体脂、生化指标及RBP4、脂联素及TNF-α水平。结果 T2DM各亚组及OW/OB-NGR组RBP4均显著高于NBM-NGR组, OW/OB-T2DM组RBP4显著高于NBM-T2DM组;T2DM各亚组及OW/OB-NGR组脂联素均显著低于NBM-NGR组;T2DM各亚组TNF-α均显著高于NBM-NGR组及OW/OB-NGR组。Spearman相关分析显示,RBP4与脂联素呈负相关,与TNF-α呈正相关,TNF-α与脂联素呈负相关（P＜0.05或0.01）。多元逐步回归分析显示,甘油三酯及腰臀比（WHR）是血清RBP4的独立相关因素;性别、甘油三酯、糖化血红蛋白（HbA1c）及高密度脂蛋白是血清脂联素的独立相关因素;HbA1c是血清TNF-α的独立相关因素。结论 RBP4与腹内型肥胖的关系更为密切,而与血糖不相关;脂联素、TNF-α主要与糖代谢相关;RBP4与脂联素及TNF-α均相关。     

Tumor necrosis factor-alpha antagonism protects from myocardial inflammation and fibrosis in experimental diabetic cardiomyopathy

To investigate the effect of anti-cytokine-based therapy in the course of diabetic cardiomyopathy, we performed a study using an anti-TNF-α monoclonal antibody treatment (mab) in Sprague male Dawley (SD) rats with streptozotocin-induced diabetic cardiomyopathy. Five days after streptozotocin injection, rats were treated with the anti-TNF-α mAb C432A for 6 weeks.At the end of the study, left ventricular (LV) function was determined by a pressure-catheter. Intercellular adhesion molecule (ICAM)-1, vascular adhesion molecule (VCAM)-1, β2-lymphocyte-integrins⁺ (CD18⁺, CD11a⁺, CD11b⁺), ED1/CD68⁺ and cytokine (TNF-α, interleukin (IL)-1β)- expressing infiltrates, total collagen content and stainings of collagen I and III were quantified by digital image analysis. LV phosphorylated and total ERK protein levels were determined by Western Blot. TNFα-antagonism reduced ICAM-1- and VCAM-1 expression and leukocyte infiltration to levels of non-diabetics and decreased macrophage residence by 3.3-fold compared with untreated diabetics. In addition, anti-TNF-α mAb-treatment decreased diabetes-induced cardiac TNF-α and IL-1β expression by 2.0-fold and 1.8- fold, respectively, and reduced the ratio of phosphorylated to total ERK by 2.7-fold. The reduction in intramyocardial inflammation was associated with a 5.4-fold and 3.6-fold reduction in cardiac collagen I and III content, respectively. This was reflected by a normalization of cardiac total collagen content to levels of non-diabetics and associated with an improved LV function. TNFα-antagonism attenuates the development of experimental diabetic cardiomyopathy associated with a reduction of intramyocardial inflammation and cardiac fibrosis.     

大鼠血清白细胞介素1β和肿瘤坏死因子α随增龄而变化

目的观察不同月龄Wistar大鼠血清白细胞介素1β(IL-1β)和TNF-α水平的变化。方法选取Wistar大鼠35只,按月龄分为4组,3月龄组(10只)、12月龄组(9只)、18月龄组(10只)和24月龄组(6只),采用放射免疫分析法分别测定4组大鼠血清IL-1β和TNF-α水平的变化。结果血清IL-1β水平在18月龄组和24月龄组大鼠明显高于3月龄组和12月龄组大鼠[(0.50±0.16)μg/L、(0.48±0.07)μg/Lvs(0.33±0.07)μg/L、(0.35±0.09)μg/L,P<0.01,P<0.05];TNF-α水平在12、18和24月龄组大鼠均较3月龄组大鼠明显升高[(2.35±0.49)μg/L、(2.97±0.46)μg/L、(3.01±0.23)μg/Lvs(1.84±0.35)μg/L,P<0.05,P<0.01]。结论血清IL-1β水平在中年(12月龄大鼠)至老年前期(18月龄)随月龄的增长而升高;TNF-α水平从青年至老年前期随月龄的增长而升高。血清炎性细胞因子在衰老过程中的变化特点说明,机体免疫调节功能的改变主要出现在老年前期,而不是老年期。     

Use of anti tumor necrosis factor-alpha monoclonal antibody for ulcerative jejunoileitis

Ulcerative jejunoileitis is an uncommon clinical syndrome consisting of abdominal pain,weight loss associated with diarrhea,and multiple inflammatory ulcerations and strictures of the small bowel.Ulcerative jejunoileitis can complicate established celiac disease or develop in patients de novo.Increased levels of tumor necrosis factor-alpha(TNF-α) in the small intestine of patients with untreated celiac disease are associated with a role in the immune pathogenesis of this disorder.No specific therapy has been shown to change the course of ulcerative jejunoileitis.We report a case of severe ulcerative jejunoileitis previously unresponsive to traditional therapies,including high dose corticosteroids and cyclosporine.The patient had a dramatic resolution of symptoms and a complete normalization of endoscopic findings after anti-TNF-α monoclonal antibody,infliximab(Remicade).