简介:·AIM:ToexploretheimmunomodulatoryeffectsofcurdlanoninnateimmuneresponsesagainstAspergillusfumigatus(A.fumigatus)inculturedhumancornealepithelialcells(HCECs),andwhetherC-typelectinreceptorDectin-1mediatestheimmunomodulatoryeffectsofcurdlan.·METHODS:TheHCECswerestimulatedbycurdlanindifferentconcentrations(50,100,200,400μg/mL)forvarioustime.ThenHCECspretreatedwithorwithoutlaminarin(Dectin-1blocker,0.3mg/mL)andcurdlanwerestimulatedbyA.fumigatushyphae.ThemRNAandproteinproductionoftumornecrosisfactor-α(TNF-α)andinterleukin-6(IL-6)weredeterminedbyreal-timequantitativepolymerasechainreactionandenzyme-linkedimmunosorbentassay,respectively.TheproteinlevelofDectin-1wasmeasuredbyWesternblot.·RESULTS:CurdlanstimulatedmRNAexpressionofTNF-αandIL-6inadoseandtimedependentmannerinHCECs.CurdlanpretreatmentbeforeA.fumigatushyphaestimulationsignificantlyenhancedtheexpressionofTNF-αandIL-6atmRNAandproteinlevelscomparedwithA.fumigatushyphaestimulationgroup(P<0.05).BothcurdlanandA.fumigatushyphaeup-regulatedDectin-1proteinexpressioninHCECs,andDectin-1expressionwaselevatedto1.5-to2-foldbycurdlanpretreatmentfollowedhyphaestimulation.TheDectin-1blockerlaminarinsuppressedthemRNAexpressionandproteinproductionofTNF-αandIL-6inducedbycurdlanandhyphae(P<0.05).·CONCLUSION:ThesefindingsdemonstratedthatcurdlanpretreatmentenhancedtheinflammatoryresponseinducedbyA.fumigatushyphaeinHCECs.Dectin-1isessentialfortheimmunomodulatoryeffectsofcurdlan.Curdlanmayhavehighclinicalapplicationvaluesinfungalkeratitistreatment.
简介:目的探讨非粒细胞缺乏肺曲霉病患者血清Dectin-1检测的临床意义。方法收集非粒细胞缺乏的曲霉病患者22例(肺曲霉病组),健康体检者54例(对照组),留取血清,ELISA方法检测两组血清Dectin-1水平。分析Dectin-1水平与血清1,3-D葡聚糖抗原检测(G试验)、半乳甘露聚糖抗原检测(GM试验)和血白细胞计数的关系。结果肺曲霉病组血清Dectin-1水平为(427.2±42.6)pg/mL,对照组为(280.8±39.4)pg/mL,差异有统计学意义(P〈0.05);Dectin-1水平与血白细胞计数、G试验、GM试验无相关性。结论在非粒细胞缺乏曲霉病患者血清中,Dectin-1水平明显增高,提示Dectin-1是重要的抗曲霉免疫分子。
简介:目的研究miR-146a是否参与新生隐球菌感染免疫应答过程.方法采用RT-PCR检测了6例新生隐球菌性脑膜炎患者和6名健康个体外周血单个核细胞(PBMC)中miR-146a的表达.以热灭活新生隐球菌刺激来自健康个体的PB-MC,并加入Dectin-1抑制剂昆布多糖,采用RT-PCR检测热灭活新生隐球菌和昆布多糖对PBMC中miR-146a表达的影响.结果新生隐球菌性脑膜炎患者PBMC中miR-146a的表达较健康个体明显增高.热灭活新生隐球菌可以上调PBMC中miR-146a的表达,昆布多糖可以削弱其上调miR-146a表达的能力.结论热灭活新生隐球菌可以通过Dectin-1受体上调miR-146a的表达.miR-146a参与了新生隐球菌感染免疫应答过程,值得进一步研究.
简介:摘要目的探讨香烟烟雾提取物(CSE)对肺泡巨噬细胞(AMs)Dectin-1受体表达及对烟曲霉感染应答能力的影响。方法实验研究。大鼠肺泡巨噬细胞株NR8383加入CSE后再使用烟曲霉静止期孢子(RC)刺激以建立烟曲霉体外感染细胞模型,流式细胞仪、激光共聚焦显微镜、蛋白质印迹检测Dectin-1表达;siRNA沉默和慢病毒载体过表达Dectin-1后通过吞噬实验检测AMs对RC吞噬能力,定量实时聚合酶链反应、酶联免疫吸附试验检测相关细胞因子表达。结果激光共聚焦显微镜(15.29±2.88比24.56±4.01,t=11.75,P<0.05)及流式细胞仪(17.73±4.95比25.94±7.12,t=17.27,P<0.05)均显示CSE降低AMs表面Dectin-1受体的表达。RC体外刺激后Dectin-1 mRNA的表达出现时间依赖性增加,对照组在所有时间点都较CSE组显著增加(P值均<0.05);蛋白表达结果类似:对照组明显高于CSE组(18 h:0.755±0.035比0.360±0.047;24 h:0.968±0.035比0.552±0.049,P值均<0.05)。CSE降低AMs对RC吞噬能力(吞噬率:53.33%±9.95%比75.17%±8.66%;吞噬指数:2.17±0.58比7.67±1.53,P值均<0.05)。siRNA下调Dectin-1表达联合CSE可以进一步降低NR8383细胞对RC的吞噬力(P<0.05),但单纯下调Dectin-1表达对RC的吞噬能力差异无统计学意义(P>0.05)。Dectin-1介导细胞因子肿瘤坏死因子α(TNF-α)、白细胞介素1β(IL-1β)和IL-4的产生:TNF-α、IL-1β在对照组增加尤为明显,感染6 h后达峰值,每个时间点比较差异均有统计学意义(P值均<0.05)。与之相反,IL-4在CSE组升高更为显著,每个时间点比较差异均有统计学意义(P值均<0.05)。IL-10表达也增加,但2组间比较差异无统计学意义(P>0.05)。使用siRNA抑制/慢病毒过表达Dectin-1对4种细胞因子mRNA和蛋白产生同向作用。结论CSE可引起AMs Dectin-1受体低表达和功能障碍,导致烟曲霉感染后吞噬能力降低和细胞因子异常表达。CSE引起的AMs抗曲霉防御能力下降部分是通过Dectin-1介导的。
简介:AIM:Toinvestigatetheexpressionofdendriticcell-associatedC-typelectin-1(dectin-1)attheearlyperiodofAspergillusfumigatusinfectioninrat’scornealepithelium.·METHODS:Atotalof72Wistarratswererandomlydividedintothreegroups:A,BandC.Therighteyeswerechosenasexperimentaleyes.GroupAwascontrolgroup.RatsingroupBwerenotinoculatedwithAspergillusfumigatus.GroupCwastakenasAspergillusfumigatuskeratitismodel.RatsingroupBandC(sixfromeachgroup)wereexecutedrandomlyat4,8,16and24hoursafterexperimentalmodelbeingestablishedtoassesstheexpressionofdectin-1mRNAthroughreal-timePCR.AnothersixratsingroupBandCwereexecutedrandomlyat24hourstoassesstheexpressionofdectin-1proteinthroughimmunohistochemistry.·RESULTS:Theresultsofreal-timePCRindicatedthatdectin-1mRNAexpressionwaslowincornealepitheliumofnormalrats’.Therewasnosignificantlydifferenceofdectin-1mRNAexpressioningroupAandB(P>0.05).TheexpressionofAspergillusfumigatusinfectedcornealepitheliumincreasedgraduallyafter8hoursingroupC.ThesynchronousexpressionofgroupAandChadsignificantdifference(P<0.01).Immunohistochemistydiscoveredthatdectin-1receptorexistedinnormalrat’scornealepithelium.Dectin-1proteinincreasedafter24hoursingroupC.TherewasasignificantdifferenceofsynchronousexpressioningroupBandC(P<0.01).·CONCLUSION:Dectin-1existsinrat’scornealepitheliumanditsexpressionsignificantlyincreasesattheearlyperiodofAspergillusfumigatusinfection.Dectin-1isapatternrecognitionreceptorthatexpressesincornealepitheliumandinvolvesinimmuneresponsetoAspergillusfungalkeratitis.
简介:β的识别;由dectin-1的-glucans被显示了调停房间激活,cytokine生产和许多抗真菌的回答。这里,我们报导在到Candidaalbicans的mucosal免疫的dectin-1的功能的活动被主人的基因背景影响。Dectin-1在C57BL/6,然而并非BALB/c老鼠为胃肠、阴道的candidiasis的合适的控制被要求;事实上,后者当dectin-1不在时显示出增加的抵抗。到感染的dectin-1-deficientC57BL/6老鼠的危险性在IL-17A和芳基烃受体依赖者IL-22生产并且在适应Th1回答与缺点被联系。相反,dectin-1-deficientBALB/c鼠标的抵抗与增加的IL-17A和IL-22生产并且向提供免疫学的存储器的Th1/Treg有免疫力的回答扭曲被联系。迥异的正规/不在经典中的NF-κ;dectin-1下游地表明小径的B在二不同老鼠紧张被激活。因此,在抗真菌的mucosal免疫的dectin-1的网活动依赖于主人的基因背景,它在dectin-1发信号之上影响天生的cytokine生产和适应Th1/Th17房间激活。
简介:你知道不莱梅吗?噢——它是一个美丽快乐的地方。不莱梅在哪儿呢?噢——有梦想的地方就有不莱梅。没错儿,不莱梅这个地方,早就存在于“很久很久以前”的童话里了……