简介：巨噬细胞有效地通过杀死肿瘤房间的一主要机制要求房间到房间接触，显示在激活的巨噬细胞的房间表面上表示的某些分子可以调停tumoricidal能力。肿瘤坏死因素(TNF)和氮的氧化物(没有)是肿瘤房间death.However的二个古典调停人，差异的证据正在积累显示这些已知的调停人不看起来说明女人和巨噬细胞的有势力tumoricidal活动。获得tumoricidalactivationassociated膜蛋白质的一个完整的全部剧目，我们把一个维的SDS页与毛状的液体chromatographytandem团spectrometry(LC-MS/MS)相结合。用这种技术，我们鉴别454激活的巨噬细胞明确地与极其高的信心表示了蛋白质，包括巨噬细胞的大多数已知的激活标记，例如没有synthase(iNOS)，Ym1，cyclooxygenase，等等。膜界限TNF-也在激活的巨噬细胞上被识别。然而，它也在thioglycolate上被检测得到的巨噬细胞，显示这个分子不能在变化形式依赖者肿瘤房间杀死起一个关键作用。相反，尽管不没作为变化形式依赖者tumoricidal小径的一个受动器分子被分配，iNOS从激活的巨噬细胞的膜部分被识别，不建议可以涉及变化形式依赖者tumoricidal机制，因为有血浆膜的iNOS协会理想地被适合直接不交付进联系肿瘤房间。这研究提供不仅新卓见进巨噬细胞变化形式依赖者tumoricidal机制，而且巨噬细胞激活的一个珍贵数据集合联系的膜蛋白质，因此在反肿瘤和另外的生物进程提供巨噬细胞的功能的机制的更好的理解。

简介：ActivinAisakindofpre-inflammatoryfactorthatbelongstothetransforminggrowthfactor-β(TGF-β)superfamily.ToinvestigatetheeffectandmechanismofactivinAontheactivitiesofmousemacrophages,thesecretionofNOinthesupernatantofculturedmouseperitonealmacrophageswasexaminedbyNOassaykit,andtheexpressionofiNOS,ActRIIAandARIP2mRNAinmouseperitonealmacrophageswasanalyzedbyRT-PCR.TheresultsshowedthatactivinAstimulatedthesecretionofNOandtheexpressionofiNOSmRNAinnon-activatedmousemacrophagesinatime-anddose-dependentmanner.Incontrast,activinAinthesameconcentrationinhibitedthesecretionofNOinLPS-activatedmousemacrophagesinadose-dependentmanner.ActRIIAwashighlyexpressedonmacrophages,andactivinAupregulatedtheActRIIAmRNAexpressioninmacrophages.Anti-ActRIIAantibodycanblockthesecretionofNOfromthemacrophagesstimulatedbyactivinA.Furthermore,RT-PCRanalysisrevealedthatactivinAenhancedtheARIP2mRNAexpressioninmacrophages.TheseresultsindicatedthatActivinAmaybeaweakactivatorcomparedwithLPStomousemacrophages,andactivinAmaymodulatethesecretionofNOthroughActRIIA-ARIP2signalpathwayinmousemacrophages.

简介：PreviousstudieshaveshownthatoligodeoxynucleotidescontainingunmethylatedCpGmotifswereusedasadjuvantsforimmunoregulationandimmuneresponse.ThisstudywastoexploretheactivationeffectsofBifidobacteriaDNAcontainingunmethylatedCpGmotifs(CpGDNA)onmurinemacrophageJ774A.1cells.ThegenomicDNAofBifidobacteriawasextractedandpurified,andthemethylationdegreeofCpGmotifswastested.Thephagocyticabilityofthemacrophageswasdetectedbyflowcytometry.Thecytokines(IL-1β,IL-6,IL-12p40andTNF-α)levelsintheculturesupernatantsofBifidobacteriaDNAtreatedJ774A.1cellswereassayedbyELISA.Thecontentofnitricoxide(NO)wasdetectedbyGriessreagent.AftertreatedwithBifidobacteriaDNAfor24h,NileRedstainincreasedinJ774A.1macrophage,whichsuggestedthatthelipidmetabolismincreasedinthemacrophages.ThephagocyticabilityandlevelsofNOandcytokinesofIL-1β,IL-6,IL-12p40andTNF-αweresignificantlyhigherthanPBSgroupandCTDNAgroup.TheresultsindicatedthatBifidobacteriaDNAcouldactivatemurinemacrophagesJ774A.1,whichcouldprovidescientificbasisfortheresearchandapplicationofmicroorganismDNApreparation.

简介：Toinvestigatetheeffectsofantisenseoligonucleotidesontheexpressionofmacrophagemigrationinhibitoryfactor(MIF)onmacrophages,themousephosphorothioateoligonucleotidesweredesignedandsynthesizedwiththesequencesofantisense,5'-TACGGATACAAGTAGCAC-3'；Sense,5'-ATGC-CTATGTTCATCGTG-3'；Missense,5'-CTCTCAGACTCGATCTGT-3'.Thesephosphorothioateoligonucleotideswerethentransfectedintoculturedmacrophages(RAW264.7)byluciferasevector,andthetransfectedmacrophageswereincubatedwithLipopolysaccharide(LPS)(1ng/ml)forvariousperiodsoftimesandcollectedafterwards.ThecontentofMIFproteinintheculturalsupernatantswasdeterminedbyELISA,cellularRNAextractedandtheexpressionofMIFmRNAwasexaminedbyRT-PCRanalysis.TheexperimentalresultsshowedthatLPScouldinduceatime-dependentspecificexpressionofMIFonmacrophages,inwhichtheMIFmRNAincellsandtheMIFproteininculturalsupernatantsappearedafter3handreachedtheirhighestconcentrationat9-12hafterLPSstimulation.ThelevelsofmRNAandproteinsinthemacrophagestreatedwithantisenseolignucleotidesweredecreasedsignificantlyafterstimulationwithLPSincomparisonwiththatofstimulationwithLPSaloneorwiththatwithLPSplussenseormissenseoligonucleotides.TherewerenodifferencesamongthosewithoutLPSstimulation.ItisconcludedthatmacrophagesstimulatedwithLPSexpressMIF,andtheantisenseolignucleotidesofMIFinhibittheexpressionofMIFmRNAaswellasthesecretionofMIFproteinsinmacrophages.

简介：ActivinA，转变生长因素贝它(TGF-)的一个多功能的因素总科，被microglia和巨噬细胞主要生产，并且它的反煽动性并且支持inflammatory活动是与巨噬细胞功能有关的两个。然而，在vivo的剩余的巨噬细胞上的activinA的直接效果仍然保持不清楚。在现在的学习，结果显示出那activinA不仅不增加了并且IL-1版本，而且在vitro并且在vivo的鼠标腹巨噬细胞的支持的吞噬细胞的能力，而它没影响MHC我和MHCII表示。而且，我们显著地发现那activinAupregulatedCD14和CD68的表情，成熟巨噬细胞的标记，在在vitro并且在vivo的巨噬细胞的表面上。这些数据建议activinA能在vitro并且在vivo导致主要巨噬细胞成熟，但是不能经由调整涉及抗原的表示的MHC分子的表示触发获得的有免疫力的反应。

简介：InordertoanalyzethemechanismofimmunomodulationbyLPSonmurineperitonealsuppressormacrophages,wehave,usingRNaseprotectionassay,checkedthechangesofmRNAexpressionpatternofseveralcytokinegenesduringtheimmuno-modulation.Ithasbeenfoundthat,aftertreatingperitonealsuppressormacrophageswithLPS,mRNAsofIL-12p35,IL-12p40,IL-6andIFN-γarenewlyappeared,whilethoseofIL-1α，IL-1βandIL-1Raareincreasebandthoseofothercytokines,likeTGF-β1andMIFarenotchangedatall.Itseemscertainthatthosecytokines,whoseexpressionisincreasedbyLPSstimulation,mayberesponsibleforthefunctionalchangesofsuppressormacrophagesduringimmuno-modulation.Amongthesechanges,theappearanceofIL-12mRNAmayplayacriticalrole,and,inthisregard,thesynergeticeffectbetewwnIFN-γandLPSontheincreaseofIL-12p35andIL-12p40mRNAexpressionisaninterestingfinding.

简介：Thisstudywasundertakentohaveabetterunderstandfortheprocessandtheunderlyingmechanismstolimitmacrophageactivationandpopulationofactivatedmacrophages.AcomprehensivekineticsofcytokineproductionwasperformedinmurineperitonealmacrophagesrecoveredfromBalb/cmiceatvarioustimeduringthecourseofanintraperitonealinjectionwiththioglycollate(TG).TheexpressionofcellsurfacemoleculessuchasMHC-Ⅰ,MHC-Ⅱ,B7-1andB7-2ofthesemacrophageswerealsodeterminedbyflowcytometry.Thepresentfindingsofourresearchsuggestedthatthepopulationofactivatedmacrophagesandtheactivationofmacrophages(includingcytokinesproductionandexpressionofcellsurfacefunctionalmolecules)werestrictlycontrolledduringinflammationprocess.Thisisoneoftheimportantmechanismstoretainthehosthomeostasis.Cellular&MolecularImmunology.2004;1(1):57-62.

简介：有免疫力的房间，特别地巨噬细胞，在导致组织缺氧的煽动性的反应起关键作用。小GTPaseRhoB被许多刺激很快通常导致并且被描述了为细胞骨架组织和泡和膜受体trafficking的一个重要管理者。然而，RhoB是否涉及导致组织缺氧的煽动性的反应，是未知的。这里，我们在巨噬细胞在RhoB表示的RhoB和机制和意义的表示上调查了组织缺氧的效果。我们显著地发现了那组织缺氧upregulated在老鼠的RAW264.7房间，鼠标腹巨噬细胞，和怒气的RhoB的表达式。RhoB的导致组织缺氧的表示被组织缺氧可诱导的factor-1(HIF-1)的一个特定的禁止者显著地堵住，c6月N终端kinase(JNK)，或细胞外信号的调整蛋白质kinase(英皇家空军之阶级最低之兵)，显示那激活组织缺氧的HIF-1，JNK，和英皇家空军之阶级最低之兵被组织缺氧涉及RhoB的upregulation。RhoB表示击倒不仅interleukin-1贝它(IL-1)的显著地压制的基础生产，interleukin6(IL-6)，并且在normoxia而且更多的肿瘤坏死因素alpha(TNF-)显著地减少了这些cytokines的刺激组织缺氧的生产。而且，我们证明RhoB增加了NF-Btranscriptional的原子factor-kappaB(NF-B)活动，和抑制活动显著地减少了IL-1，IL-6，和TNF-的增加RhoB的mRNA层次。最后，我们证明RhoB提高了房间粘附并且在normoxia和组织缺氧禁止了房间移植。一起拿，这些结果建议RhoB在巨噬细胞和煽动性的反应的导致组织缺氧的激活起一个重要作用。

简介：AbstractPurpose:The combined use of antibiotics and anti-inflammatory medicine to manage bacterial endotoxin-induced inflammation following injuries or diseases is increasing. The cytokine level produced by macrophages plays an important role in this treatment course. Ciprofloxacin and indomethacin, two typical representatives of antibiotics and anti-inflammatory medicine, are cost-effective and has been reported to show satisfactory effect. The current study aims to investigate the effect of ciprofloxacin along with indomethacin on the secretion of inflammatory cytokines by macrophages in vitro.Methods:Primary murine peritoneal macrophages and RAW 264.7 cells were administrated with lipopolysaccharide (LPS) for 24 h. The related optimal dose and time point of ciprofloxacin or indomethacin in response to macrophage inflammatory response inflammation were determined via macrophage secretion induced by LPS. Then, the effects of ciprofloxacin and indomethacin on the secretory functions and viability of various macrophages were determined by enzyme-linked immunosorbent assay and flow cytometry analysis, especially for the levels of interleukin (IL)-1β, IL-6, IL-10, and tumor necrosis factor (TNF)-α. The optimal dose and time course of ciprofloxacin affecting macrophage inflammatory response were determined by testing the maximum inhibitory effect of the drugs on pro-inflammatory factors at each concentration or time point.Results:According to the levels of cytokines secreted by various macrophages (1.2 × 106 cells/well) after administration of 1 μg/mL LPS, the optimal dose and usage timing for ciprofloxacin alone were 80 μg/mL and 24 h, respectively, and the optimal dose for indomethacin alone was 10 μg/mL. Compared with the LPS-stimulated group, the combination of ciprofloxacin and indomethacin reduced the levels of IL-1β (p < 0.05), IL-6 (p < 0.05), IL-10 (p < 0.01)), and TNF-α (p < 0.01). Furthermore, there was greater stability in the reduction of inflammatory factor levels in the combination group compared with those in which only ciprofloxacin or indomethacin was used.Conclusion:The combination of ciprofloxacin and indomethacin suppressed the levels of inflammatory cytokines secreted by macrophages in vitro. This study illustrates the regulatory mechanism of drug combinations on innate immune cells that cause inflammatory reactions. In addition, it provides a new potential antibacterial and anti-inflammatory treatment pattern to prevent and cure various complications in the future.

简介：巨噬细胞在免疫和动态平衡起一个重要作用。在经由特定的受体的病原体识别之上，他们很快导致煽动性的回答。这个过程紧在transcriptional水平被控制。DNA有约束力的锌手指蛋白质CCCTC有约束力的因素(Ctcf)是远程的染色质相互作用的一个关键管理者并且协调在抄写因素和基因表达式进程之间的特定的通讯。在这研究，Ctcf基因被使用转基因的Cre-LoxP系统明确地在myeloid房间删除。在myeloid房间的Ctcf基因的有条件的删除在vivo导致了温和显型。显著地展出的Ctcf缺乏的老鼠减少了主要histocompatibility的表示在肝的建筑群(MHC)班II。Ctcf缺乏的巨噬细胞表明了正常表面显型和吞噬作用能力。在像使用费的受体(TLR)之上刺激，他们生产了支持inflammatorycytokinesIL-12和IL-6的正常层次，但是表明了一个强烈损害的能力生产肿瘤坏死因素(TNF)和IL-10，以及表示IL-10家庭成员IL-19，IL-20和IL-24。一起拿，我们的数据表明涉及巨噬细胞功能调整的Ctcf的一个角色。

简介：TheimmunomodulatingeffectsofF12onmouseperitonealmacroplhageswasintendedtobestudiedwithdifferentdosesof20,40,80,and120mg/Kg.F12increasedperoxidaseactivityindexcdependentmammerfrom0.02±0.001,to0.175±0.038,0.211±0.041,0.137±0.045and0.078±0.036,respectively,increasedcytotoxicityfrom127.33±22.96to162.74±19.53,237.30±25.15,178.62±36.22and158.66±42.75dpm,respectively,promotedphagocyticactivityfrom0.03±0.01to0.21±0.016,0.43±0.041,0.40±0.032and0.30±0.160^b,Furthermore,F12inaconcentrationof15,30,60,120ug/mlenhancedIL-1productionfrom0.15±0.02to0.20±0.005^b0.21±0.02,0.22±0.005,0.24±0.002and0.22±0.02,respectively,ThusF12canbeconsideredasaneffectivestimulatorofmacrophages.

简介：瞄准：为了检验因素，用一个最近确定的在试管内模型在肠的巨噬细胞(IMAC)的区别包含了。方法：测试是否可溶或膜界限因素induceIMAC区别，刚，elutriated单核白血球(瞬间)与肠的上皮细胞(IEC)的调节媒介或细胞膜被孵化或与在transwell系统的IEC有教养。决定瞬间的活跃迁居的重要性，从瞬间和IEC的1:1混合的三维的总数被免疫组织化学和流动血细胞计数检验。Apoptosis被caspase-3检验西方的污点。在区别模型的细胞外的矩阵生产被免疫组织化学比较。结果：IMAC区别在一个复杂三维的合作文化模型被观察(多细胞的球状体，MCS)与在进球状体的瞬间的移植以后的IEC。由有调节媒介或IEC的膜准备的瞬间的合作文化，没有IMAC区别被导致。有在transwell文化的IEC的瞬间的合作文化，与二个房间，膜也分开的人口没导致瞬间的象肠一样区别。与有在IEC和瞬间的混合MCS入境瞬间的IEC球状体相对照，瞬间的一张仅仅小潜水艇人口能熬过七个天文化时期。结论：瞬间在试管内的象肠一样区别仅仅在三维的MCS在在IMAC的区别期间显示房间矩阵或房间房间相互作用的一个角色的瞬间的移民以后建模的建筑群被导致。

简介：AbstractAcute kidney injury (AKI), characterized by acute renal dysfunction, is an increasingly common clinical problem and an important risk factor in the subsequent development of chronic kidney disease (CKD). Regardless of the initial insults, the progression of CKD after AKI involves multiple types of cells, including renal resident cells and immune cells such as macrophages. Recently, the involvements of macrophages in AKI-to-CKD transition have garnered significant attention. Furthermore, substantial progress has also been made in elucidating the pathophysiological functions of macrophages from the acute kidney to repair or fibrosis. In this review, we highlight current knowledge regarding the roles and mechanisms of macrophage activation and phenotypic polarization, and transdifferentiation in the development of AKI-to-CKD transition. In addition, the potential of macrophage-based therapy for preventing AKI-to-CKD transition is also discussed.

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简介：TheaimofthisstudyistoelucidatethemolecularandcellularmechanismsunderlyingtheimmunosuppressiveeffectofSanchiextract(SE)viainvestigatingtheeffectsofSEontheactivationandproliferationofmurinelymphocytesandNOsecretionbyperitonealmacrophagesinvitro.ConAwasusedtoactivatelymphocytes,andexpressionofCD69onTcellsandCFSElabeledcelldivisionweredetectedbyflowcytometry.MurineperitonealmacrophageswerestimulatedwithLPSorlymphocytesculturesupemate(LCS)andtheconcentrationofNOwasdeterminedbyGriessreagentassay.After6hofculture,SErangingfrom50to100μg/mldownregulatedCD69expressiononConA-activatedTcells,whileSErangingfrom12.5to100μg/mlinhibitedtheproliferativeresponseoflymphocytestoConA.Additionally,SE(12.5-100μg/ml)inhibitedsecretionofNObyperitonealmacrophagesstimu-latedbyLPSorLCS.ThisstudyrevealsthatSEinhibitstheactivationandproliferationofmurinelym-phocytesandNOsecretionbyperitonealmacrophages.

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简介：ObjectivesToexploretheprotectiveeffectofirbesartan(Irb)undertheinterferencewithangiotensinⅡ(AngⅡ)onABCA1.MethodsElectronmicroscopywasusedtodetectthemorphousoffoamcells.TheexpressionofABCA1mRNAanditsproteinweredeterminedbyRT-PCRandWesternblotting,respectively.Thevarianceofcellularcholesterolcontentwasmeasuredbyzymochemistryvia-fluorospectrophotometer.ResultsApositivefacilitativeeffectofAngⅡontheformationoffoamcellswasobserved.TotalcholesterolwasincreasedsignificantlybyAngⅡ,theexpressionofABCA1wasdown-regulatedobviouslybyAngⅡ;IrbcouldprotectABCA1againstthelesionofAngⅡ;TotalcellularcholesterolcontentwasreducedsignificantlyinIrb+AngⅡgroup;However,considerablealterationaboutthecholesterolcontentandtheexpressionofABCA1werenotobservedinIrbgroupwithoutincubationwithAngⅡ.ConclusionsIrbcouldprotectABCA1againstthelesionofAngⅡ,whichmaycontributetoitsanti-atheroscleroticproperties.

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：AbstractObjective:This study was designed to evaluate whether p62/SQSTM1 (hereafter referred to as p62) is involved in the immune response of macrophages against challenge by Candida albicans (C. albicans).Methods:We cultured bone marrow-derived macrophages (BMDMs) to investigate the immune response to challenge by C. albicans. The p62 gene was knocked down by transfection with p62 small interfering RNA (siRNA) in the p62 siRNA group. BMDMs transfected with nonsense siRNA served as the negative control (NC) group. These two groups of BMDMs were challenged with C. albicans in vitro. We detected p62 expression through quantitative reverse transcription PCR and western blotting. The phagocytosis ability of BMDMs was evaluated by flow cytometry and microscopic examination using an Olympus FV1000 laser scanning confocal microscope. Moreover, we determined the level of reactive oxygen species (ROS) in BMDMs. The mRNA levels of proinflammatory cytokines were determined by quantitative reverse transcription PCR.Results:After stimulation by C. albicans, the relative expression of p62 mRNA was increased in a dose-dependent manner, the relative expression of p62 and the ratio of BMDMs to C. albicans is 1.893 ± 0.2156 (1:1, P < 0.05), 2.873 ± 0.4787 (1:3, P < 0.05) and 3.556 ± 0.2892 (1:5, P < 0.01). The p62 protein level was also increased. After transfection with p62 siRNA, the mRNA and protein levels of p62 were significantly decreased in BMDMs (P < 0.05). After 0.5, 1 and 2 hours of co-culture of BMDMs with C. albicans, flow cytometry showed that the phagocytosis rates of C. albicans by BMDMs were significantly lower in the p62 siRNA group than in the NC group (39.70 ± 1.69% vs. 55.23 ± 0.72%, 46.70 ± 0.89% vs. 60.80 ± 1.78%, 51.90 ± 0.98% vs. 64.43 ± 2.0%, respectively, all P < 0.05). Consistent results were seen in the production of ROS (4269 ± 392.6 vs. 13426 ± 1859.7, 4967 ± 721.2 vs. 13687 ± 2611.2, 7647 ± 1950.0 vs. 17719 ± 1814.2, respectively, all P < 0.05). The ROS levels were higher in BMDMs of the NC group than in BMDMs transfected with p62 siRNA at 0.5, 1, and 2 hours after treatment with C. albicans. BMDMs was co-cultured with C. albicans for 4 and 12 hours, the mRNA levels of interleukin-1β and interleukin-18 in NCs were also higher than p62 siRNA group, interleukin-1β: (6.14 ± 1.63 vs. 12.12 ± 0.54, 8.81 ± 0.86 vs. 26.2 ± 4.67, respectively, all P < 0.05), IL-18: (0.38 ± 0.02 vs. 0.97 ± 0.06, 0.44 ± 0.02 vs. 2.23 ± 0.46, respectively, all P < 0.05).Conclusion:p62 plays an important role in the process of phagocytosis in BMDMs challenged by C. albicans through ROS production and expression of proinflammatory cytokines.