以肠内营养为主的综合营养方法对溃疡性结肠炎患者肠道菌群含量与细胞因子、TLRs表达量的影响

[目的]探讨以肠内营养为主的综合营养方法对溃疡性结肠炎(UC)患者肠道菌群含量与细胞因子、TLRs分子表达量的影响。[方法]选取我院2018年1月～2019年1月收治的80例UC患者作为研究对象,按照随机数字法分为观察组(n=40)和对照组(n=40),其中对照组仅实施常规的对症治疗与肠外治疗,而观察组则实施以肠内营养为主的综合营养方案。分别对2组患者的肠道菌群含量与细胞因子、TLRs分子表达量进行客观比较。[结果]干预前后,观察组与对照组的乳酸杆菌、肠球菌、链球菌、双歧杆菌、类杆菌、葡萄球菌、消化球菌、酵母菌、梭杆菌和大肠杆菌等含量比较差异有统计学意义(P0.05);观察组干预后的IL-6和TNF-α等炎性因子指标明显更低于对照组和干预前,差异有统计学意义(P0.05),而对照组干预后的IL-10和IL-4水平则相对观察组更高(P0.05);另外,2组间的TLR2、TLR4、TLR5和TLR9表达量差异有统计学意义(P0.05)。[结论]以肠内营养为主的综合营养方案有助于改善UC患者肠道菌失调,减少致炎细胞因子以及助于增加TLR的含量,具备推广优势。     

肠道菌群及IL-23/IL-17轴与溃疡性结肠炎的相关性分析

目的分析肠道菌群、白细胞介素-23(IL-23)/白细胞介素-17(IL-17)轴与溃疡性结肠炎严重程度的相关性。方法选取2015年6月至2019年6月连云港市第二人民医院收治的100例溃疡性结肠炎患者为溃疡性结肠炎组,另选同期100例健康体检者为对照组,对两组以及溃疡性结肠炎组内不同分型患者肠道菌群(肠杆菌、肠球菌、酵母菌、双歧杆菌、乳杆菌)、IL-17、IL-23进行对比,利用Spearman相关性分析法对肠道菌群、IL-17、IL-23与溃疡性结肠炎严重程度的相关性进行检验。结果溃疡性结肠炎组肠杆菌、肠球菌、IL-17、IL-23高于对照组,酵母菌、双歧杆菌、乳杆菌低于对照组,差异有统计学意义(P<0.05);溃疡性结肠炎组内轻型患者肠杆菌、肠球菌、IL-17、IL-23最低,酵母菌、双歧杆菌、乳杆菌最高,重型患者肠杆菌、肠球菌、IL-17、IL-23最高,酵母菌、双歧杆菌、乳杆菌最低,中型介于其间,各组间差异有统计学意义(P<0.05);Spearman相关性分析结果提示,肠杆菌、肠球菌与IL-17、IL-23呈正相关性(P<0.05),酵母菌、双歧杆菌、乳杆菌与IL-17、IL-23呈负相关性(P<0.05),肠杆菌、肠球菌与溃疡性结肠炎严重程度呈正相关性(P<0.05),酵母菌、双歧杆菌、乳杆菌与溃疡性结肠炎严重程度呈负相关性(P<0.05),IL-17、IL-23与溃疡性结肠炎严重程度呈正相关性(P<0.05)。结论肠道菌群,IL-23/IL-17轴与溃疡性结肠炎之间存在着密切的关联性,或可能为该病症的重要治疗靶点。     

重组人生长激素对重症急性胰腺炎肠黏膜屏障、肠道菌群及炎症因子的影响

目的探讨重组人生长激素对重症急性胰腺炎(severe acute pancreatitis,SAP)肠黏膜屏障、肠道菌群及炎症因子的影响。方法选择湖北医药学院附属人民医院2012年6月-2016年2月收治的80例SAP患者作为研究对象,按随机数字表分为观察组(43例)与对照组(37例)。对照组采取常规综合治疗并应用生长抑素粉针剂,观察组在对照组基础上加用重组人生长激素冻干粉针剂。比较两组治疗前后小肠黏膜绒毛高度、陷窝深度、肠杆菌、双歧杆菌、乳酸杆菌、IL-6、IL-8、TNF-α。结果治疗前两组小肠黏膜绒毛高度、陷窝深度、肠杆菌、双歧杆菌、乳酸杆菌、IL-6、IL-8、TNF-α比较,差异无统计学意义(P0.05);与治疗前相比,对照组治疗后小肠黏膜绒毛高度与陷窝深度差异均无统计学意义(P0.05),观察组治疗后小肠黏膜绒毛高度及陷窝深度均高于治疗前及对照组治疗后(P0.05)。治疗后两组肠杆菌数量、IL-6、IL-8、TNF-α降低,双歧杆菌及乳酸杆菌增多(P均0.05),治疗后观察组肠杆菌数量、IL-6、IL-8、TNF-α低于对照组,双歧杆菌及乳酸杆菌多于对照组(P均0.05)。结论重组人生长激素在SAP患者中的应用可减轻肠黏膜损伤,修复胃肠道黏膜,调整肠道菌群,抑制早期细胞因子的瀑布效应,下调IL-6、IL-8、TNF-α,抑制炎症进展,从而促进病情缓解。     

非酒精性脂肪性肝病患者血清TLR4、IL-10、IL-22与肠道菌群的相关性

目的探讨非酒精性脂肪性肝病(NAFLD)患者血清Toll样受体4(TLR4)、白介素-10(IL-10)、白介素-22(IL-22)与肠道菌群的相关性。方法研究对象选自2016年6月至2018年8月期间我院消化内科收治的126例NAFLD患者。选取同期进行体检的健康人90例作为对照组。比较各组间肠道菌群及肠道定植抗能力,血清TLR4、IL-10、IL-22水平,并进行pearson相关性分析和logistic多元回归分析。结果与对照组相比,NAFLD组双歧杆菌、乳酸杆菌、B/E值更低(P0.05),肠杆菌、肠球菌更高(P0.05)。NAFLD组血清TLR4显著高于对照组,IL-10、IL-22低于对照组(P0.05)。经pearson相关性分析,NAFLD患者TLR4与双歧杆菌、乳酸杆菌、B/E值呈负相关(P0.05),与肠杆菌、肠球菌呈正相关(P0.05);IL-10、IL-22与双歧杆菌、乳酸杆菌、B/E值呈正相关(P0.05),与肠杆菌、肠球菌呈正负相关(P0.05)。经logistic回归分析发现,TLR4、IL-10、IL-22是NAFLD患者B/E值的影响因素。结论 TLR4、IL-10、IL-22可能通过影响NAFLD患者的肠道菌群失调,参与疾病的发生、发展。     

溃疡性结肠炎患者血清TNF-α、IL-10表达与肠道菌群分布的相关性

目的观察溃疡性结肠炎(UC)患者肠道菌群分布情况,分析血清肿瘤坏死因子-α(TNF-α)、白细胞介素-10(IL-10)水平与肠道菌群的关系,为未来该类疾病临床干预方案的制定提供参考依据。方法回顾性分析2017年1月至2020年6月南京医科大学附属南京医院(南京市第一医院)完成治疗的29例活动期UC患者,作为观察组;并选取同期院内完成治疗的29例缓解期UC患者,作为对照组;对比分析两组血清TNF-α、IL-10表达与肠道菌群分布情况,分析各血清指标与肠道菌群的关系。结果观察组血清TNF-α水平高于对照组,且血清IL-10水平低于对照组,差异有统计学意义(P<0.05);观察组乳杆菌、梭杆菌数量均多于对照组,且双歧杆菌、拟杆菌数量均少于对照组,差异有统计学意义(P<0.05);相关性分析结果显示,血清TNF-α水平与乳杆菌、梭杆菌均呈正相关(r>0,P<0.05),与双歧杆菌、拟杆菌均呈负相关(r<0,P<0.05);血清IL-10水平与乳杆菌、梭杆菌均呈负相关(r<0,P<0.05),与双歧杆菌、拟杆菌均呈正相关(r>0,P<0.05)。结论UC患者普遍存在肠道菌群分布异常的情况,可能与血清TNF-α、IL-10异常表达相关,临床可通过早期持续监测UC患者的血清TNF-α、IL-10水平,以评估其肠道菌群分布情况,指导早期合理干预。     

益生菌对白血病化疗后继发腹泻患者的影响

目的研究益生菌辅助应用对急性淋巴细胞白血病化疗后继发腹泻患者肠黏膜屏障功能及炎性细胞因子水平的影响.方法选择2015-01/2016-12在台州市立医院治疗的化疗相关性腹泻患者90例.随机分为对照组(n=45)和观察组(n=45),对照组患者在常规对症支持治疗的基础上加用蒙脱石散,观察组患者在对照组的基础上加用双歧杆菌三联活菌胶囊.比较两组患者的临床疗效、肠黏膜屏障功能、炎性细胞因子水平及肠道菌群等.结果观察组患者显效25例(55.56%),有效17例(37.78%),总有效率为93.33%,对照组总有效率为75.56%(P0.05).治疗前两组患者的肠黏膜屏障功能指标水平相近(P0.05),治疗后两组患者的二胺氧化酶(d i a m i n e oxidase,DAO)、D-乳酸和内皮素(endothelin,ET)水平均明显下降,观察组患者的DAO、D-乳酸和ET水平低于对照组(P0.05).治疗前两组患者的炎性细胞因子水平相近(P0.05),治疗后两组患者的肿瘤坏死因子-?(tumor necrosis factor alpha,TNF-?)、降钙素原(procalcitonin,PCT)和白介素(interleukin,IL)-6水平均明显下降,观察组患者的TNF-?、PCT和IL-6水平低于对照组(P0.05).对照组治疗后的肠道菌群数值较治疗前明显降低,观察组治疗后双歧杆菌、乳杆菌较治疗前明显增多,观察组治疗后肠道菌群数值明显高于对照组(P0.05),观察组肠杆菌、肠球菌、大肠埃希菌数值治疗前后相近(P0.05).结论双歧杆菌辅助应用可以明显提高急性淋巴细胞白血病患者化疗相关性腹泻的临床疗效,降低炎性细胞因子水平,改善肠黏膜屏障功能,调节肠道菌群平衡紊乱,重建肠道生态平衡,值得在临床推广.     

青春双歧杆菌对溃疡性结肠炎患者血清相关因子的影响

目的研究青春双歧杆菌对溃疡性结肠炎(UC)患者血清相关因子的影响。方法采用酶联免疫吸附试验(ELISA)法检测UC患者治疗前后及正常对照组血清肿瘤坏死因子(TNF)-α,干扰素(IFN)-γ,白细胞介素(IL)-6及IL-10的水平,并分别比较各组细胞因子水平的差异。结果UC患者血清TNF-α、IFN-γ、IL-6水平明显高于正常对照组,而IL-10水平明显低于正常对照组(P0.05);传统治疗组及双歧杆菌治疗组血清TNF-α、IFN-γ、IL-6水平较治疗前下降,而IL-10水平较治疗前升高(P0.05),两治疗组与正常对照组相比无明显差异(P0.05)。结论青春双歧杆菌可以降低UC患者血清促炎因子TNF-α、IFN-γ及IL-6水平,还可升高抑炎因子IL-10水平,调节肠黏膜的细胞免疫功能,可用于UC的治疗。     

益生菌对实验性结肠炎大鼠Toll样受体4表达的影响

目的 观察两种益生菌(乳酸杆菌、双歧杆菌)对溃疡性结肠炎的大鼠结肠黏膜Toll样受体4(TLR4)及TNT-α的变化及影响.方法 采用三硝基苯磺酸/乙醇与免疫复合物联合诱导溃疡性结肠炎大鼠模型.观察和评估其结肠黏膜的大体和组织学变化.以免疫组化方法检测TIR4、TNF-α的表达,以蛋白免疫印迹法检测蛋白表达.结果 造模后结肠组织中可见大量炎性细胞浸润,杯状细胞减少,隐窝脓肿形成.与正常对照组相比,模型组结肠组织TLR4的表达显著增加(P＜0.01).TNF-α表达显著升高(P＜0.01);与益生菌组相比,模型组结肠组织TLR4的表达显著减少(P＜0.01),TNF-α表达显著减少(P＜0.01).其两种菌相比差异不大(P＞0.05).结论 从免疫机制的视角观察到益生菌可能通过抑制Toll样受体4表达从而减少炎性因子TNF-α产生.     

肠道微生态对三硝基苯磺酸诱导大鼠结肠炎肠黏膜上皮细胞紧密连接蛋白occludin保护作用的研究

目的研究肠道微生态对三硝基苯磺酸(trinitro-benzen-sulfonic acid,TNBS)诱导大鼠结肠炎肠黏膜上皮细胞紧密连接蛋白的保护作用。方法建立TNBS诱导大鼠结肠炎模型。实验分为正常组、模型组和双歧杆菌嗜酸乳杆菌肠球菌三联活菌(金双歧)组。进行疾病活动指数(DAI)和组织学损伤评分,用ELISA法测定结肠组织TNF-α、IL-10和血清内毒素水平,采用免疫组织化学染色检测紧密连接(tight junction,TJ)相关蛋白occludin的分布。结果TNBS诱导大鼠结肠炎后,DAI和组织学损伤评分增高,结肠组织TNF-α水平升高,IL-10水平降低和血清内毒水平升高,而经双歧杆菌嗜酸乳杆菌肠球菌三联活菌处理后,DAI和组织学损伤评分有明显下降,结肠组织TNF-α水平降低,IL-10水平升高和血清内毒素水平降低,组间比较差异有显著性(P0.05)。TNBS诱导大鼠结肠炎后,TJ结构遭到破坏,TJ相关蛋白的表达亦减少,而双歧杆菌嗜酸乳杆菌肠球菌三联活菌(金双歧)处理后可使TNBS引起的TJ结构受损减轻,相关蛋白的表达增多(P0.05)。结论肠道微生态对TNBS诱导大鼠结肠炎肠黏膜上皮细胞TJ蛋白具有明显的保护作用,其可能的机制是通过纠正肠道微生态,上调肠上皮细胞TJ蛋白occludin的表达,降低结肠组织TNF-α水平,提高IL-10水平,从而抑制内毒素通过紧密连接进入体循环。     

嗜酸乳杆菌La28对新生大鼠坏死性小肠结肠炎肠道菌群及肠道免疫功能的影响

目的 探究嗜酸乳杆菌La28对新生大鼠坏死性小肠结肠炎(necrotizing enterocolitis, NEC)肠道菌群及肠道免疫功能的影响。方法 51只新生大鼠随机分出10只作为对照组，其余大鼠建立NEC模型，最终存活36只，随机分为模型组、La28组与双歧杆菌组，每组12只。La28组与双歧杆菌组每日接受2次对应菌配方奶灌胃，每次0.1 ml,对照组与模型组接受等体积普通配方奶灌胃，连续7 d。干预结束后处死所有大鼠，观察组织学变化，免疫荧光检测组织Beclin-1、LC3Ⅱ表达情况，ELISA检测血清DAO、D-LA水平，检测TNF-α、IL-6、IL-1β水平。采集盲肠内容物，16S rRNA高通量测序检测肠道菌群相对含量。流式细胞术检测组织CD4/CD8比值，Western blotting检测组织ZO-1、Occludin、Claudin-1、Claudin-2表达情况。结果 模型组肠道明显可见肠壁变薄、积气，肠黏膜绒毛脱落，黏膜下层分离，黏膜下层和肌层水肿，细胞形态异常；La28组、双歧杆菌组肠道外观较模型组有所改善。与对照组相比，模型组、La28组、双歧杆菌组NE...     

培菲康对实验性溃疡性结肠炎大鼠TNF-α、IL-10水平的影响

目的阐明培菲康对三硝基苯磺酸钠(TNBS)诱导的大鼠溃疡性结肠炎(UC)TNF-α、IL-10水平的影响,寻求UC治疗的有效新途径。方法成年雌性SD大鼠50只,随机分成5组(n=10):正常对照组(G1)、模型对照组(G2)、培菲康治疗组(G3)、奥沙拉嗪治疗组(G4)、培菲康和奥沙拉嗪联合治疗组(G5),经不同处理和治疗后,通过免疫组化染色观测各组大鼠结肠组织中TNF-α(两步法)、IL-10(S-P法)表达情况,通过实时荧光定量PCR分析结肠组织中TNF-α、IL-10mRNA的表达水平。结果G1组各指标显著低于G2组(P0.001),肠组织结构正常;与G2组相比,G3、G4、G5组TNF-α、IL-10细胞阳性率和TNF-α、IL-10mRNA的表达水平显著降低(P0.001);与G3或G4组相比,G5组TNF-α、IL-10细胞阳性率和TNF-α、IL-10mRNA的表达水平也显著降低(P0.001);G3或G4组之间,TNF-α、IL-10细胞阳性率及TNF-αmRNA水平无差别(P0.05),而G4组IL-10mRNA水平明显低于G3组(P0.001)。结论TNF-α、IL-10在溃疡性结肠炎(UC)的发生、发展过程中起重要作用,培菲康能明显降低该过程中肠组织TNF-α、IL-10的表达水平,可能通过调控这两个细胞因子的表达而发挥疗效。     

US government restrictions lead to limited access to weight-loss surgery in patients most in need

Evaluation of: Frolova L, Drastich P, Rossmann P, Klimesova K, Tlaskalova-Hogenova H. Expression of Toll-like receptor 2 (TLR2), TLR4, and CD14 in biopsy samples of patients with inflammatory bowel diseases: upregulated expression of TLR2 in terminal ileum of patients with ulcerative colitis. J. Histochem. Cytochem. 56(3), 267–274 (2007).

Inflammatory bowel disease (IBD) consists of Crohn’s disease, which involves not only the large intestine but also the small intestine, and ulcerative colitis, which only involves the large intestine. The dysregulation of innate and adaptive intestinal immune responses to bacterial microbiota is believed to be highly involved in the pathogenesis of IBD. Toll-like receptors (TLRs) play a key role in microbial recognition in innate immunity and control the adaptive immune responses. Among the TLRs, TLR2 recognizes bacterial lipoprotein and peptidoglycan, whereas TLR4 and its coreceptor, CD14, recognize lipopolysaccharide. The expression levels of TLR2 or TLR4 have been shown to be limited in the intestine of healthy volunteers, suggesting a minimalization of the recognition of microbiota in the intestinal lumen. The paper under evaluation highlighted the expression levels of TLR2, TLR4 and CD14 in the terminal ileum, cecum and rectum of IBD patients (19 Crohn’s disease and 20 ulcerative colitis patients) and of 20 healthy volunteers. The authors suggested that the dysregulation of TLR2, TLR4 and CD14 expression in different parts of the intestinal mucosa might, therefore, play a crucial role in the pathogenesis of IBD.     

萝卜硫素对慢阻肺患者TLR4、MyD88以及下游炎性因子的影响分析

目的探讨萝卜硫素对慢性阻塞性肺病(简称:慢阻肺)患者Toll样受体(TLR4)、髓样分化因子88(My D88)及炎性因子的影响作用。方法选取40例稳定期慢阻肺患者作为病例组,同期健康体检者40例作为健康组,采集患者外周静脉血,分离单核细胞,诱导形成单核细胞源性巨噬细胞(MDM),将MDM分为脂多糖、萝卜硫素、萝卜硫素+脂多糖、及不处理(空白组)。健康组不给予任何处理措施,采用实时荧光聚合酶链反应(PCR)检测TLR4 mRNA、My D88 mRNA,免疫荧光染色法检测TLR4、My D88蛋白,采用ELISA法检测炎性因子肿瘤坏死因子-ɑ(TNF-ɑ)、白细胞介素-6(IL-6)。结果慢阻肺患者的TLR4 mRNA、My D88 mRN、蛋白表达到水平显著高于健康组(P0.05),不同处理方式下慢阻肺患者TLR4 mRNA、My D88 mRNA、蛋白表达水平组间比较为脂多糖组空白组萝卜硫素+脂多糖萝卜硫素组且差异均具有统计学意义(P0.05)。慢阻肺患者的TNF-ɑ、IL-6表达水平显著的高于健康组(P0.05),不同处理方式下慢阻肺患者TNF-ɑ、IL-6表达水平组间比较结果为脂多糖组空白组萝卜硫素+脂多糖萝卜硫素组且差异均具有统计学意义(P0.05)。结论慢阻肺患者的外周血巨噬细胞Toll样受体(TLR4)、髓样分化因子88(My D88)高表达,萝卜硫素可以降低TLR4、My D88、高表达,从而减轻慢阻肺患者的炎症反应。     

Characteristics of intestinal dendritic cells in inflammatory bowel diseases

BACKGROUND & AIMS: Dendritic cells (DCs) recognize and respond to microbial structures using pattern recognition receptors, including Toll-like receptors (TLRs). In the intestine, DCs are pivotal in tolerance induction and direct the differentiation of T cells. We aimed to identify changes in intestinal DCs that may underlie the dysregulated immune response to enteric bacteria that occurs in patients with inflammatory bowel disease (IBD). METHODS: DCs were identified in freshly isolated lamina propria mononuclear cells by multicolor flow cytometry in patients with IBD and controls. Expression of TLR2, TLR4, and the activation/maturation marker CD40 was assessed by cell surface labeling. Production of cytokines (interleukin [IL]-12, IL-6, and IL-10) was assessed in the absence of exogenous stimulation by intracellular staining of permeabilized cells. RESULTS: In healthy controls, few intestinal DCs expressed TLR2 or TLR4, in contrast to blood DCs. DC expression of both TLRs was significantly enhanced in Crohn's disease and ulcerative colitis. DCs from inflamed tissue of patients with Crohn's disease expressed significantly higher levels of the maturation/activation marker CD40. Elevated levels of CD40 on DCs were decreased after treating patients with anti-tumor necrosis factor alpha. In Crohn's disease, but not ulcerative colitis, more colonic DCs produced IL-12 and IL-6. The number of IL-10-producing DCs did not differ significantly between patients with IBD and controls. CONCLUSIONS: In IBD, DCs are activated, their expression of microbial recognition receptors is up-regulated, and more DCs produce pathologically relevant cytokines. Intestinal DCs are likely to be key initiators or perpetuators of the inflammatory response that characterizes IBD.     

微生态制剂对实验性大鼠结肠炎的治疗

目的 评价微生态制剂双歧三联活菌对三硝基苯磺酸钠(TNBS)诱导的大鼠结肠炎的疗效,探索炎症性肠病(IBD)治疗的新方法.方法 成年雌性SD大鼠50只,随机分为对照组(G1)、模型组(G2)、双歧三联活菌治疗组(G3)、奥沙拉秦治疗组(G4)、双歧三联活菌和奥沙拉秦联合治疗组(G5),每组10只.ELISA法检测各组的血清C反应蛋白(CRP)、TNFα、IL-10水平,分光光度法检测肠组织髓过氧化物酶(MPO)活力,并对肠组织进行病理组织学分析.结果 治疗后,G1组肠组织结构正常,血清CRP、TNFα、IL-10水平、结肠黏膜损伤指数(CMDI)及肠组织MPO活力显著低于G2组(P<0.001);G2组肠组织炎症程度最莺,血清CRP、TNFα、IL-10水平、CMDI及肠组织MPO活力最高,P<0.05;3个治疗组G3、G4、G5组的肠组织炎症呈不同程度消散,血清CRP、TNFα、IL-10水平及肠组织MPO活力呈不同程度下降,以G5组最显著,P<0.05;G2组血清CRP、TNFα、IL-10及肠组织MPO活力均分别与CMDI呈正相关,P<0.001.结论 双歧三联活菌能有效改善TNBS诱导的大鼠结肠炎,其机制可能与调节细胞因子水平有关.     

Epstein–Barr Virus DNA Exacerbates Colitis Symptoms in a Mouse Model of Inflammatory Bowel Disease

Infection with EBV has been associated with various inflammatory disorders including inflammatory bowel diseases (IBD). Contribution of this virus to intestinal disease processes has not been assessed. We previously detected that EBV DNA triggers proinflammatory responses via the activation of endosomal Toll-like receptor (TLR) signaling. Hence, to examine the colitogenic potential of EBV DNA, we used the dextran sodium sulfate (DSS) mouse colitis model. C57BL/6J mice received either DSS-containing or regular drinking water. Mice were then administered EBV DNA by rectal gavage. Administration of EBV DNA to the DSS-fed mice aggravated colonic disease activity as well as increased the damage to the colon histologic architecture. Moreover, we observed enhanced expression of IL-17A, IFNγ and TNFα in colon tissues from the colitis mice (DSS-treated) given the EBV DNA compared to the other groups. This group also had a marked decrease in expression of the CTLA4 immunoregulatory marker. On the other hand, we observed enhanced expression of endosomal TLRs in colon tissues from the EBV DNA-treated colitis mice. These findings indicate that EBV DNA exacerbates proinflammatory responses in colitis. The ubiquity of EBV in the population indicates that possible similar responses may be of pertinence in a relevant proportion of IBD patients.     

哮喘患儿治疗前后血清不同促炎因子和抗炎因子水平改变的临床意义研究

目的探讨哮喘患儿治疗前后血清不同促炎因子和抗炎因子水平改变的临床意义。方法连续性收录80例哮喘急性发作患儿,综合分析比较治疗前后血清促炎因子(IFNγ,TNFα,IL-1β以及Il-6)和抗炎因子(IL-10,TGFβ以及IL-4)水平改变。结果哮喘患儿治疗前血清IFNγ,TNFα以及IL-6等促炎因子水平高于对照组(P0.05)。经治疗后,血清IFNγ和Il-6水平下降最为明显(P0.05)。哮喘患儿治疗前血清IL-10和IL-4等抗炎因子水平低于对照组(P0.05)。经治疗后,血清IL-10和IL-4水平上升最为明显(P0.05)。危重亚组患儿血清IFNγ和IL-6水平明显高于轻度亚组(P0.05)。哮喘分级和促炎因子TNFα呈负相关(r=-0.589,P0.05)。促炎因子TNFα与IL-6(r=0.599,P0.05),IL-1β与IL-6(r=0.532,P0.05)之间存在正相关。促炎因子TNFα与抗炎因子TGFβ呈负相关(r=-0.662,P0.05)。结论哮喘患儿血清IFNγ、IL-6、IL-10和IL-4水平在治疗过程中动态变化,与哮喘严重程度密切相关。     

Differences in the Expression of TLRs and Inflammatory Cytokines in Pre-Eclamptic Compared with Healthy Pregnant Women

Background: Preeclampsia (PE) is one of the most complex and life-threatening pregnancy disorders and is considered as a major cause of mortality among mothers and fetuses worldwide. Although the exact etiology of PE is not well known several lines of evidence support an immunological etiology for PE. Objective: To investigate the differences in the expression of TLRs 2, 4, 5, and 6 and a group of inflammatory cytokines including IL-1, IL-6, TNF-α and IFN-γ in placentas from PE and healthy pregnant women in their third trimester of pregnancy. Methods: This case-control study was performed on fifteen PE and fifteen age and gestational matched healthy pregnant women in the third trimester of pregnancy. Real time PCR (RT-PCR) technique was used to determine the expression of TLRs 2, 4, 5, and 6 in the maternal and fetal parts of the placenta. Moreover, the expressions of IL-1, IL-6, TNF-α and IFN-γ at RNA level in placental samples, peripheral, and cord blood were investigated. Results: The results of the present study indicated that the expressions of TLRs 4, 5 and 6 were significantly increased in both maternal part (p<0.001 and p<0.003 for TLRs 4, 6 and TLR 5, respectively) and fetal part (p<0.001), while TLR2 showed significant increase only in the fetal part of PE placentas (p<0.002). The levels of all studied cytokines showed over-expression within peripheral and cord blood samples from PE patients (p<0.001 for IL-1, IL-6, and IFN-γ and p<0.004 for TNF-α in both cord and peripheral blood samples). Conclusion: The finding of the present study indicated that the expression of the studied TLRs and inflammatory cytokines are generally suppressed in normal pregnancy, but are up regulated in preeclamptic women. Moreover, it seems that the maternal and fetal parts of the placenta may play different roles in the induction of the inflammatory status within the placenta.     

感染旋毛虫小鼠不同时期TLR2/TLR4 mRNA表达量及血清炎性因子的变化

目的 探讨旋毛虫感染对小鼠不同组织细胞TLR2/ TLR4（Toll样受体）表达量及血清炎性因子的影响.方法 分别取感染前、后不同时期小鼠心肌、肺及腹腔巨噬细胞,应用半定量PCR方法检测TLR2/ TLR4 mRNA相对表达量,同时应用ELISA方法对血清相关炎性因子进行检测.结果 随着旋毛虫感染时间的变化,TLR4和TLR2在心肌、肺和腹腔巨噬细胞上的表达略有不同,但大致呈双峰状.旋毛虫感染初期4d左右,TLR2/ TLR4 mRNA表达均有不同程度升高,之后降低,14 d左右,心肌与肺TLR升高,巨噬细胞TLR则继续下降,在21 d左右,心肌TLR表达量达到最高值,且与对照组差异显著（P＜0.05）,肺组织TLR呈下降趋势,巨噬细胞TLR表达升高,之后下降并趋于稳定.感染鼠的血清中炎性因子IL 2和NO的表达量显著升高（P＜0.05）,而TNF-α、IL-10和IL-12的表达量则显著降低（P＜0.05）,IL-6的表达量变化不明显.结论 旋毛虫感染可引起小鼠心肌、肺和巨噬细胞上的Toll样受体TLR2/TLR4表达发生变化,继而调节相关细胞因子分泌也发生变化,这种变化与旋毛虫生活史不同阶段抗原及其引起的宿主免疫反应和组织器官损伤具有一定相关性.