Interleukin 1βreceptor and synaptic dysfunction in recurrent brain infection with Herpes simplex virus type-1

Several experimental evidence suggests a link between brain Herpes simplex virus type-1 infection and the occurrence of Alzheimer’s disease.However,the molecular mechanisms underlying this association are not completely understood.Among the molecular mediators of synaptic and cognitive dysfunction occurring after Herpes simplex virus type-1 infection and reactivation in the brain neuroinflammatory cytokines seem to occupy a central role.Here,we specifically reviewed literature reports dealing with the impact of neuroinflammation on synaptic dysfunction observed after recurrent Herpes simplex virus type-1 reactivation in the brain,highlighting the role of interleukins and,in particular,interleukin 1βas a possible target against Herpes simplex virus type-1-induced neuronal dysfunctions.

Gossypol acetic acid regulates leukemia stem cells by degrading LRPPRC via inhibiting IL-6/JAK1/STAT3 signaling or resulting mitochondrial dysfunction

BACKGROUND Leukemia stem cells(LSCs)are found to be one of the main factors contributing to poor therapeutic effects in acute myeloid leukemia(AML),as they are protected by the bone marrow microenvironment(BMM)against conventional therapies.Gossypol acetic acid(GAA),which is extracted from the seeds of cotton plants,exerts anti-tumor roles in several types of cancer and has been reported to induce apoptosis of LSCs by inhibiting Bcl2.AIM To investigate the exact roles of GAA in regulating LSCs under different microenvironments and the exact mechanism.METHODS In this study,LSCs were magnetically sorted from AML cell lines and the CD34+CD38-population was obtained.The expression of leucine-rich pentatricopeptide repeat-containing protein(LRPPRC)and forkhead box M1(FOXM1)was evaluated in LSCs,and the effects of GAA on malignancies and mitochondrial RESULTS LRPPRC was found to be upregulated,and GAA inhibited cell proliferation by degrading LRPPRC.GAA induced LRPPRC degradation and inhibited the activation of interleukin 6(IL-6)/janus kinase(JAK)1/signal transducer and activator of transcription(STAT)3 signaling,enhancing chemosensitivity in LSCs against conventional chemotherapies,including L-Asparaginase,Dexamethasone,and cytarabine.GAA was also found to downregulate FOXM1 indirectly by regulating LRPPRC.Furthermore,GAA induced reactive oxygen species accumulation,disturbed mitochondrial homeostasis,and caused mitochondrial dysfunction.By inhibiting IL-6/JAK1/STAT3 signaling via degrading LRPPRC,GAA resulted in the elimination of LSCs.Meanwhile,GAA induced oxidative stress and subsequent cell damage by causing mitochondrial damage.CONCLUSION Taken together,the results indicate that GAA might overcome the BMM protective effect and be considered as a novel and effective combination therapy for AML.

大黄对烫伤大鼠肝脏内细胞因子基因表达的影响

目的：观察大黄在创伤后系统炎症反应中对肝脏内细胞因子基因表达的影响，揭示大黄“清热解毒”的药理机制。方法：采用大鼠２５％ 体表面积Ⅲ度烫伤模型，应用随机、前瞻性研究方法进行观察。烫伤后１２ 小时经静脉持续输注内毒素予以“二次打击”，总剂量为２０ ｍ ｇ／ｋｇ。观察大黄对肝脏内肿瘤坏死因子（ＴＮＦ α）、白介素 １β（ＩＬ １β）基因表达的影响，以及对门、体静脉血内毒素的清除作用。结果：正常对照组和单纯烫伤组肝脏内ＴＮＦ α、ＩＬ １β无明显表达，“二次打击”后肝内ＴＮＦ α、ＩＬ １β基因表达明显增加；大黄可明显抑制肝脏内ＴＮＦ α、ＩＬ １β基因表达，与正常对照组、单纯烫伤组和烫伤加内毒素组比较均有显著性差异（Ｐ均＜０．００５）。烫伤可使肠道内毒素吸收入血，门静脉血中内毒素含量明显高于体静脉血（Ｐ＜ ０．０５）。“二次打击”后门、体静脉血中内毒素浓度更高，但两者浓度差消失。大黄治疗后门、体静脉血中内毒素浓度显著下降（Ｐ＜０．０１）。结论：大黄可抑制创伤和后继“二次打击”后肝脏内ＴＮＦ α、ＩＬ １β基因表达。

白介素-1β及其受体拮抗蛋白在肠缺血-再灌注所致急性肺损伤中的作用研究

目的 :探讨肠缺血再灌注 ( I/R)损伤时肺损伤的机制和白介素 1β及其受体拮抗蛋白 ( IL 1ra)的作用。方法 :用大鼠肠系膜上动脉夹闭造成 I/R损伤模型 ,利用放射免疫分析法测定损伤前后和各处理组血液、肺组织灌洗液中 IL 1β和 IL 1ra水平。同时采用逆转录聚合酶链反应 ( RT PCR)法测定肺组织中 IL 1β和IL 1ra m RNA的表达含量。经光镜和电镜观察肺局部白细胞浸润及组织损伤情况。结果 :I/R损伤后 6小时血液中 IL 1β和 IL 1ra有所增加 ,损伤组 IL 1β比对照组明显增加 ,而 IL 1ra不明显 ;但损伤组和对照组IL 1ra伤后 6小时比伤前自身对照组均明显增加。损伤组肺灌洗液中 IL 1β明显增多 ,而 IL 1ra不明显。肺组织中 IL 1β的 m RNA在损伤后表达明显增加 ,而 IL 1ra表达没有明显变化。经非特异性磷脂酶 A2( PLA2 )阻断剂 (氯喹和三氟拉嗪 )、血小板活化因子受体阻断剂 SR2 7417A、环氧化酶抑制剂消炎痛以及抗氧化剂愈创木酸等处理后 ,血清、肺灌洗液和肺组织中上述指标有不同程度的改变。肺内白细胞的聚集和浸润明显减少。结论 :IL 1β和 IL 1ra可能参与肠 I/R介导的急性肺损伤 ,并且和局部 PLA2

芹菜素抑制IL-1和脂多糖诱导软骨细胞产生NO

目的：研究植物黄酮芹菜素对ＩＬ－１、脂多糖（ＬＰＳ）诱导软骨细胞产生一氧化氮（ＮＯ）的抑制作用。方法：ＩＬ－１，ＬＰＳ体外诱导兔软骨细胞产生ＮＯ。以一氧化氮合酶（ＮＯＳ）抑制剂Ｎ－硝基－Ｌ－精氨酸做对照，研究芹菜素对产生ＮＯ的抑制作用。结果和结论：芹菜素（３．１２５～２５μｍｏｌ／Ｌ）剂量依赖性地抑制ＩＬ－１或ＬＰＳ诱导的ＮＯ产生，其抑制作用强于Ｎ－硝基－Ｌ－精氨酸。

实验性急性心肌梗塞时白细胞介素1的变化及其意义

探讨急性心肌梗塞时白细胞介素１（ＩＬ１）的变化及其意义。用ＭＴＴ细胞增殖法观察了８只兔在冠状动脉结扎后１小时和２小时其外周血ＩＬ１水平的变化，并与冠状动脉假结扎的８只兔作比较。结果显示：单核细胞ＩＬ１水平于结扎后１小时及２小时均较假结扎组显著增高（Ｐ＜０．００２，Ｐ＜０．００１），其峰值与同时测定的血白细胞计数呈密切的线性正相关（ｒ＝０．９０４４，Ｐ＜０．００５），与同时测定的心肌磷酸肌酸激酶同功酶（ＣＰＫＭＢ）活性呈密切的线性负相关（ｒ＝０．８９６０，Ｐ＜０．００５）。提示：急性心肌梗塞（ＡＭＩ）时ＩＬ１的升高可能是促成血白细胞增多和参与心肌ＣＰＫＭＢ活性降低的主要因素之一，因此抑制或对抗ＩＬ１的药物对减轻心肌的缺血性损伤可能有益。

温肾益心丹对充血性心力衰竭炎症细胞因子水平的影响

目的:观察温肾益心丹结合西医基础治疗对充血性心力衰竭(CHF)患者的临床疗效及其对白细胞介素1(IL1)、IL6和肿瘤坏死因子α(TNFα)的影响。方法:31例CHF患者按照住院顺序随机分为对照组和研究组,根据美国纽约心脏学会(NYHA)心功能分级方法分级,并制定统一疗效判定标准。对照组予常规西医治疗;研究组在西医常规治疗剂量1/2～2/3基础上加服温肾益心丹;疗程均为2周。治疗前后对患者的心功能及临床症状进行观测,记录并采集血标本,用酶联免疫吸附法(ELISA)检测血清IL1、IL6和TNFα含量。结果:研究组:治疗后患者NYHA心功能分级有所改善(总有效率达81.25%),血清IL6和TNFα水平则明显下降(P均<0.001),IL1治疗后也有下降,但差异无显著性(P>0.05)。对照组:治疗后患者NYHA心功能分级也有所改善(总有效率达73.33%),血清IL1、IL6和TNFα水平均有下降,但较治疗前差异无显著性(P均>0.05)。两组治疗后比较,研究组血清IL6和TNFα下降更显著(P均<0.05),血清IL1水平两组间差异无显著性(P>0.05)。结论:温肾益心丹结合西医治疗能有效改善CHF患者的心功能,降低CHF患者血清中IL6和TNFα水平,且优于单纯西医治疗。提示温肾益心丹对血清IL6和TNFα浓度水平的抑制可能是其发挥治疗作用的机制之一。

清除血液中内毒素、肿瘤坏死因子和白细胞介素-1对实验性内毒素休克时肺损伤的保护作用

目的：了解内毒素（ＬＰＳ）、肿瘤坏死因子（ＴＮＦ）和白细胞介素１（ＩＬ１）对实验性内毒素休克时肺损伤的保护作用。方法：实验分３组：Ⅰ组为假灌流组，Ⅱ组、Ⅲ组大鼠在内毒素休克早期开始分别给予活性炭（Ⅱ组）、大孔树脂ＡｍｂｅｒｌｉｔｅＸＡＤ７（Ⅲ组）血液灌流，结果与Ⅰ组作比较。结果：Ⅱ组ＬＰＳ、ＩＬ１水平明显降低，而Ⅲ组ＴＮＦ水平明显降低。Ⅱ组、Ⅲ组外周血白细胞数分别为（４．０±０．４）×１０９／Ｌ和（３．９±０．４）×１０９／Ｌ，均明显高于Ⅰ组〔（３．１±０．２）×１０９／Ｌ〕，Ｐ均＜０．０１；支气管肺泡灌洗液（ＢＡＬＦ）中的白细胞数〔（８．５±０．１）×１０９／Ｌ，（８．９±０．１）×１０９／Ｌ〕、肺系数（０．６４±０．０６，０．６６±０．０６）以及肺组织浸润的中性分叶核粒细胞数（２９．６±７．９／ＨＰ，３４．５±４．１／ＨＰ）均明显低于Ⅰ组〔（１２．３±１．８）×１０９／Ｌ，０．７５±０．０７，４８．６±６．６／ＨＰ〕，Ｐ均＜０．０１或＜０．０５。Ⅱ组、Ⅲ组的肺组织学改变亦较Ⅰ组明显减轻。结论：清除血液中致病介质可能对内毒素休克时的肺损伤产生保护作用。

苦参碱对纤维蛋白纤维蛋白原降解产物诱导血管细胞损伤、增殖及腹腔巨噬细胞释放IL-1的影响

目的：研究苦参碱（Ｍａｔ）对纤维蛋白纤维蛋白原降解产物（ＦＦＤＰ）作用的影响。方法：大鼠主动脉内皮细胞损伤以乳酸脱氢酶释放测定；大鼠主动脉平滑肌细胞增殖采用结晶紫染色法测定；白细胞介素１活性采用小鼠胸腺细胞增殖法测定。结果：ＦＦＤＰ能促进大鼠主动脉内皮细胞释放乳酸脱氢酶，诱导大鼠主动脉平滑肌细胞增殖，并促使小鼠腹腔巨噬细胞分泌ＩＬ１增加。结论：Ｍａｔ可抑制ＦＦＤＰ的作用。对动脉粥样硬化的防治可能有一定意义。

癫痫患儿血白细胞介素-1β、可溶性白细胞介素-2受体和肿瘤坏死因子-α含量的研究

目的：探讨癫痫的免疫学发病机制。方法：选择原发性全身型癫痫呈强直和（或）阵挛发作患儿６０例为研究对象，分为服用苯巴比妥、卡马西平及未服药３组，测定其外周血单核细胞（ＰＢＭＣ）在植物血凝素（ＰＨＡ）的作用下释放白细胞介素１β（ＩＬ１β）、肿瘤坏死因子α（ＴＮＦα）的量及血清ＴＮＦα、可溶性白细胞介素２受体（ＳＩＬ２Ｒ）的含量，并与对照组比较。结果：３组癫痫患儿间各指标含量均无显著性差异（Ｐ均＞０．０５），但均明显高于对照组（Ｐ＜０．０５～０．００１）。结论：癫痫患儿ＰＢＭＣ释放ＩＬ１β、ＴＮＦα的量及血清ＳＩＬ２Ｒ、ＴＮＦα含量的明显增高可能是由于细胞免疫异常等所致，其增高的幅度与是否进行抗癫痫治疗。

白细胞介素1β致痫对脑内Gas蛋白和cAMP含量变化的影响

目的 探讨白细胞介素 1 β(IL 1 β)致痫或促痫的细胞内信号转导机制。 方法 动物行为学观察、免疫细胞化学方法和放射免疫分析法。 结果 行为学观察表明 :IL 1 β组大鼠有轻至中度癫痫发作 ,IL 1 β和谷氨酸(Glu)联合注射组有中至重度癫痫发作 ,IL 1受体拮抗剂 (IL 1ra)预处理可减轻或抑制癫痫发作。IL 1 β致痫或促痫时 ,大脑皮质和海马神经元Gas蛋白免疫反应明显增强 ,海马组织cAMP含量明显增高 ,IL 1ra预处理 ,则可抑制cAMP的升高。 结论 IL 1 β可能有致痫和促进Glu致痫作用 ,IL 1ra可抑制此作用。IL 1 β致痫或促痫的细胞内信号转导机制在海马区与Gas蛋白介导的AC cAMP途径可能有密切关系。

儿童变应性鼻炎与细胞因子的相关性研究

目的：探讨儿童变应性鼻炎与细胞因子及免疫球蛋白的关系。方法：采用ＥＬＩＳＡ双抗体夹心法及单向免疫扩散试验，对４０例变应性鼻炎患儿进行了血清白细胞介素１（ＩＬ１）、白细胞介素２（ＩＬ２）及免疫球蛋白的测定，同时设健康同龄儿３０例为对照组。结果：变应性鼻炎组ＩＬ１、ＩｇＥ明显增高，ＩＬ２降低，与对照组比较有非常显著差异（Ｐ＜０．０１），ＩｇＧ、ＩｇＡ、ＩｇＭ无显著性差异（Ｐ＞０．０５）。结论：检测ＩＬ１、ＩＬ２、ＩｇＥ能对变应性鼻炎的诊断、治疗提供客观指标。

Associations between interleukin-1 polymorphisms and gastric cancers among three ethnicities

AIM:To investigate the associations between interleukin(IL)-1B and IL-1RN polymorphisms and gastric cancers among the Tibet,Hui and Han ethnicities.METHODS:Genomic DNA was extracted from peripheral blood of 210,205,and 202 healthy volunteers and from 155,158,and 197 gastric cancer patients from the Tibet,Hui,and Han populations,respectively.Polymorphisms in IL-1B and IL-1RN were analyzed by denaturing high-performance liquid chromatography.RESULTS:Carriers of the IL-1B-31 CC genotype had an increased risk of intestinal type gastric cancer [odds ratio(OR) = 2.17,P = 0.037] in the Tibet ethnicity.Carriers of the IL-1B 2/L genotype had an increased risk of both intestinal and diffuse types of gastric cancer(OR = 2.08,2.31,P = 0.007,0.016,respectively) in the Hui ethnicity.In the Han population,carriers of the IL-1B-31 CC,IL-1B-511CT,TT genotypes had increased risk of intestinal type gastric cancer(OR = 2.51,2.74,5.66,P = 0.005,0.002,0.000,respectively).CONCLUSION:IL-1B and IL-RN genotypes may differentially contribute to gastric cancer among the Tibet,Hui,and Han ethnicities in the Qinghai area of China.

Vitamin D differentially regulates Salmonella-induced intestine epithelial autophagy and interleukin-1β expression

AIM To investigate the effects of active vitamin D3 on autophagy and interleukin(IL)-1β expression in Salmonella-infected intestinal epithelial cells(IECs).METHODS Caco-2 cells, NOD2 siR NA-, Atg16L1 siR NA- or vitamin D receptor(VDR) siR NA-transfected Caco-2 cells were pretreated with 1,25-dihydroxyvitamin D3(1,25D3), and then infected by wild-type S. typhimurium strain SL1344. The conversion of LC3-I to LC3-II was detected by Western blot analysis and LC3+ autophagosome was analyzed by immunofluorescence. Caco-2 cells or VDR si RNA-transfected cells were pretreated with 1,25D3, and then infected by SL1344. Membrane protein and total RNA were analyzed by Western blot and RT-PCR for VDR and Atg16L1 protein and m RNA expression, respectively. Atg16L1 si RNA-transfected Caco-2 cells were pretreated by 1,25D3 and then infected with SL1344. Total RNA was analyzed by RT-PCR for IL-1β mR NA expression.RESULTS The active form of vitamin D, 1,25D3, showed enhanced VDR-mediated Atg16L1 mR NA expression, membranous Atg16L1 protein expression leading to autophagic LC3 II proteins expression and LC3 punctae in Salmonella-infected Caco-2 cells which was counteracted by Atg16L1 and VDR si RNA, but Atg16L1 mediated suppression of IL-1β expression. Thus, active vitamin D may enhance autophagy but suppress inflammatory IL-1β expression in Salmonella-infected IECs.CONCLUSION Active vitamin D might enhance autophagic clearance of Salmonella infection, while modulation of inflammatory responses prevents the host from detrimental effects of overwhelming inflammation.

Lipopolysaccharide induces and activates the Nalp3 inflammasome in the liver

AIM:To examine the activation of the Nalp3 inflammasome and its downstream targets following lipopolysaccharide(LPS) -induced stimulation in the liver. METHODS:Six-to-eight-week-old C57BL/6 chow fed mice were injected intraperitoneally with 0.5μg/g bodyweight LPS and sacrificed 2,4,6,18 or 24 h later. LPS-induced liver damage was confirmed by a biochemical assay to detect alanine aminotransferase(ALT) levels.To determine if LPS stimulation in the liver led to activation of the inflammasome,real-time quantitative polymerase chain reaction was used to evaluate the mRNA expression of components of the Nalp3 inflammasome.Enzyme-linked immunosorbent assays were used to determine the protein expression levels of several downstream targets of the Nalp3 inflammasome,including caspase-1 and two cytokine targets of caspase-1,interleukin(IL) -1βand IL-18. RESULTS:We found that LPS injection resulted in liver damage as indicated by elevated ALT levels.This was associated with a significant increase in both mRNA and protein levels of the proinflammatory cy-tokine tumor necrosis factor(TNF) -αin the liver,as well as increased levels of TNFs in serum.We showed that LPS stimulation led to upregulation of mRNA levels in the liver for all the receptor components of the inflammasome,including Nalp3,Nalp1,pannexin-1 and the adaptor molecule apoptosis-associated specklike,caspase recruitment domain-domain containing protein.We also found increased levels of mRNA and protein for caspase-1,a downstream target of the inflammasome.In addition,LPS challenge led to increased levels of both mRNA and protein in the liver for two cytokine targets of caspase-1,IL-1βand IL-18. Interestingly,substantial baseline expression of pre-IL1βand pre-IL-18 was found in the liver.Inflammasome and caspase-1 activation was indicated by the significant increase in the active forms of IL-1βand IL-18 after LPS stimulation. CONCLUSION:Our results show that the Nalp3 inflammasome is upregulated and activated in the liver in response to LPS stimulation.

促炎因子白细胞介素-1参与缺氧/复氧损伤的体外研究

目的研究促炎因子IL-1参与缺氧/复氧损伤的可能机制 ,探讨保护缺氧/复氧损伤的方法。方法ECV304 细胞株接种于培养瓶中 ,随机分为A、B、C、D四组 ,D为正常对照组 ,A组为实验组 ,行缺氧 (60min)/复氧 (240min)培养 ,B、C组分别与IL-1和IL-1α受体拮抗剂共孵育。测定各组细胞的成活率 ,并应用细胞免疫组化分析ECV304 细胞表面黏附分子的表达水平。结果经不同试剂培养后 ,各组细胞的成活率明显不同 ,A、B组显著低于D组 ,尤以B组为最 ;细胞形态学也发生相应改变 ;H/R孵育后ECV304 细胞株表达ICAM -1和E -selectin增加 ,外源性IL-1可以进一步上调ICAM -1和E -selectin的表达 ,而IL-1受体拮抗剂则可明显抑制这种增多现象。结论缺氧/复氧损伤过程中产生的内源性IL-1在调控ICAM -1和E-selectin的表达及中性粒细胞的黏附中发挥着重要作用 ;采取措施降低IL-1的生物学活性 。

VEGF局部动脉注射对大鼠断肢再植成活的影响及作用机制

目的:探讨血管内皮生长因子(VEGF)局部动脉注射对大鼠后肢断肢再植术后的早期影响,并观察其对血清碱性成纤维生长因子(b FGF)、白介素-1β(IL-1β)及肿瘤坏死因子-α(TNF-α)表达的影响。方法:选用健康Wistar大鼠80只,随机分为VEGF组(观察组)、低分子右旋糖酐组(对照组)、模型组、空白组,造后肢断肢再植模型,取腓肠肌标本进行HE染色,检测术前、灌注后即刻、恢复血运1天、恢复血运7天共4个时相标本丙二醛(MDA)、超氧化物歧化酶(SOD)、三磷酸腺苷酶(ATP),ELISA法检测血清b FGF、IL-1β及TNF-α表达情况。结果:1.VEGF组减少血管内膜损伤,血栓形成,镜下炎性水肿较轻。2.VEGF局部动脉注射显著增强血清b FGF分泌、降低IL-1β及TNF-α水平(P<0.05)。3.4个不同时相VEGF局部动脉注射能有效抑制MDA释放,增强SOD活性,保护骨骼肌细胞的ATP酶活力(P<0.05)。结论:VEGF局部动脉注射能有效减轻断肢再植缺血再灌注损伤,提高断肢的成活率及断肢再植的成活质量。

白细胞介素-1β与幽门螺杆菌相关性胃病

幽门螺杆菌(Helicobacter pylori,HP)是慢性活动性胃炎的主要病因,与萎缩性胃炎及胃癌发生有密切相关。HP感染可引起胃黏膜的多种细胞因子和化学趋化因子升高,而造成胃黏膜的病理改变,其中白细胞介素-1β(IL-1β)的表达与HP相关性胃病发生的危险性有明显关系。

白细胞介素-1刺激人子宫肌细胞产生前列腺素的初步研究

为观察子宫肌细胞中白细胞介素－１（ＩＬ－１）与前列腺素物质（ＰＧｓ）合成的关系，对人子宫肌细胞进行体外培养。对单层融合细胞用ＩＬ－１和一种蛋白激酶Ｃ激活剂（Ｔｅｔｒａｄｅ－ｃａｎｏｙｌｐｈｏｒｈｏｒｂｏｌａｃｅｔａｔｅ，ＴＰＡ）刺激后，于不同时间取细胞培养液，进行前列腺素Ｅ２（ＰＧＥ２）、６－酮－前列环素（６－Ｋｅｔｏ－ＰＧＩ）和环磷酸鸟甙（ｃＧＭＰ）的放免测定。实验结果表明，ＩＬ－１和ＴＰＡ分别明显促进ＰＧｓ的合成，并且有显著的协同作用。推测两者在作用环节上有所不同。证实细胞免疫因子ＩＬ－１与女性生殖系统的ＰＧｓ的产生密切相关，其在细胞内的作用与ＩＰ和ＤＡＧ第二信使途径及ｃＧＭＰ途径有关。本实验证实人子宫肌细胞不仅是ＰＧｓ的靶细胞。

严重烧伤患者血液单核细胞体外产生白细胞介素-1量的变化及临床意义

目的：检测严重烧伤患者伤后血液单核细胞体外产生白细胞介素１（ＩＬ１）量的变化，并结合内脏功能损害、多器官衰竭（ＭＯＦ）和严重全身感染的发生情况探讨其意义。方法：采用生物法检测２４例严重烧伤患者伤后不同时间单个器官功能损害患者、ＭＯＦ患者、局部感染患者和严重全身感染患者及３０例正常人单核细胞体外产生ＩＬＬ的量。结果：烧伤患者伤后单核细胞产生ＩＬ１的量减少，且病情越重，减少越多，在ＭＯＦ患者尤为明显；ＩＬ１产生量的变化与患者心、肝酶呈明显负相关。结论：ＩＬ１在严重烧伤患者内脏功能损害及ＭＯＦ的发生发展中起着重要作用。