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Lung epithelial cell-der.ved IL-25 negatively r.gulates LPS-induced exosome r.lease fr.m macr.phages

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Militar. Medical r.sear.h 2018年第4期5卷 324-334页

作者： Zhi-Gang Li Melanie J. Scott Tomasz Br.óska Pr.thu Sundd Yue-Hua Li timothy r. billiar Mar. A. Wilson Ping Wang Jie Fan Depar.ment of Sur.er. University of Pittsburgh School of MedicinePittsburgh PA 15213 USA r.sear.h and Development Veterans Affairs Pittsburgh Healthcare System Pittsburgh PA 15240 USA Hear. Lung Blood and Vascular Medicine Institute University of Pittsburgh Pittsburgh PA 15213 USA McGowan Institute for.r.gener.tive Medicine University of Pittsburgh Pittsburgh PA 15219USA The Feinstein Institute for.Medical r.sear.h Manhasset NY11030 USA.

Backgr.und: Acute lung injur.(ALI) is a major.component of multiple or.an dysfunction syndr.me(MODS) following pulmonar. and systemic infection. Alveolar.macr.phages(AMφ) ar. at the center.of ALI pathogenesis. Emer.ing evidence has shown that cell-cell inter.ctions in the lungs play an impor.ant r.gulator. r.le in the development of acute lung inflammation. However. the under.eath mechanisms r.main poor.y addr.ssed. In this study, we explor. a novel function of lung epithelial cells(LEPCs) in r.gulating the r.lease of exosomes fr.m AMφ following LPS ***: For.the in vivo exper.ments, C57 BL/6 wildtype(WT) mice wer. tr.ated with lipopolysacchar.de(LPS)(2 mg/kg) in 0.2 ml of saline via intr.tr.cheal aer.sol administr.tion. Br.nchoalveolar.lavage fluid was collected at 0–24 h after.LPS tr.atment, and exosomes der.ved fr.m AMφ wer. measur.d. For.the in vitr. studies, LEPCs and bone mar.owder.ved Mφ(BMDM) wer. isolated fr.m WT or.TLr.-/-mice and wer. then cocultur.d in the Tr.nswell? system. After.cocultur. for.0–24 h, the BMDM and super.atant wer. har.ested for.the measur.ment of exosomes and ***: We demonstr.te that LPS induces macr.phages(Mφ) to r.lease exosomes, which ar. then inter.alized by neighbor.ng Mφ to pr.mote TNF-α expr.ssion. The secr.ted inter.eukin(IL)-25 fr.m LEPCs downr.gulates r.b27 a and r.b27 b expr.ssion in Mφ, r.sulting in suppr.ssed exosome r.lease and ther.by attenuating exosome-induced TNF-α expr.ssion and ***: These findings r.veal a pr.viously unidentified cr.sstalk pathway between LEPCs and Mφ that negatively r.gulates the inflammator. r.sponses of Mφ to LPS. Modulating IL-25 signaling and tar.eting exosome r.lease may pr.sent a new ther.peutic str.tegy for.the tr.atment of ALI.

关键词： Acute lung injur. Sepsis Multiple or.an failur. r.b27

Immune Activation in the Liver.by Nucleic Acids

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Jour.al of Clinical and Tr.nslational Hepatology 2016年第2期4卷 151-157页

作者： Qian Sun Qingde Wang Melanie J.Scott timothy r.billiar Depar.ment of Sur.er. University of PittsburghPittsburghPAUSA

Vir.l infection in the liver.including hepatitis B vir.s (HBV) and hepatitis C vir.s (HCV) infection,is a major.health pr.blem wor.dwide,especially in developing *** infection tr.gger. a pr.-inflammator. r.sponse in patients that is cr.cial for.host *** studies have identified multiple tr.nsmembr.ne and cytosolic r.ceptor. that r.cognize pathogen-der.ved nucleic acids,and these r.ceptor. ar. essential for.dr.ving immune activation in the *** addition to sensing DNA/r.A fr.m pathogens,these intr.cellular.r.ceptor. can be activated by nucleic acids of host or.gin in r.sponse to ster.le *** this r.view,we discuss the expanding r.les of these r.ceptor. in both immune and nonimmune cells in the liver.

关键词： Nucleic acid Innate immunity Intr.cellular.r.ceptor Hepatocytes

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氨甲蝶呤抑制小鼠巨噬细胞一氧化氮合酶表达

基础医学与临床 2002年第3期22卷 247-250页

作者：刘质泽 timothy r.billiar 北京中日友好医院普外科北京100029 The Depar.ment of Sur.er. School of Medicine Univer.ity of Pittsbur.h Pennsylvania

研究氨甲蝶呤 (MTX)在小鼠巨噬细胞 (r.W2 6 4 7)对一氧化氮合酶 (NOS)表达的抑制作用。本试验应用内毒素 (LPS)、干扰素 (IFNr.、MTX、二氨基羟基嘧啶 (DAHP) ,四氢生物喋呤 (BH4 )刺激 8h后 ,用Nor.her.杂交检测NOSmr.A水平和GTP C... 详细信息

研究氨甲蝶呤 (MTX)在小鼠巨噬细胞 (r.W2 6 4 7)对一氧化氮合酶 (NOS)表达的抑制作用。本试验应用内毒素 (LPS)、干扰素 (IFNr.、MTX、二氨基羟基嘧啶 (DAHP) ,四氢生物喋呤 (BH4 )刺激 8h后 ,用Nor.her.杂交检测NOSmr.A水平和GTP CH 1mr.A水平表达 ,并用Gr.essr.action方法检测NO2- NO3- 浓度 ,用Duch方法测定GTP CH 1活性值。我们发现 ,MTX在小鼠巨噬细胞 (r.W2 6 4 7)对NOSmr.A水平和GTP CH 1mr.A水平表达有轻度抑制作用 ,对NO2- NO3- 浓度和GTP CH 1活性抑制作用较弱。MTX和DAHP联合应用不仅对NOSmr.A水平和GTP CH 1mr.A水平表达抑制作用较强 ,而且对NO2- NO3 浓度和GTP CH 1活性抑制较大。BH4的加入可以减少MTX和DAHP对一氧化氮 (NO)生成的抑制作用。

关键词：抑制作用氨甲蝶呤小鼠巨噬细胞一氧化氮合酶

The hepatotoxic effect of bile acids can be lar.ely attr.buted to dir.ct i nflammasome activation in hepatocytes and Kupffer.cells

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The hepatotoxic effect of bile acids can be largely attribut...

r.le of tr.nscr.ption factor.Egr.1 in liver.injur. following hemor.hagic shock and r.suscitation

2015年浙江省外科学学术年会暨国家级肝胆胰疾病诊治进展学习班

作者： Xiqiang Liu Tonghui Ma timothy r.billiar Dongsheng Huang r.n Tao Center.for.Or.an Tr.nsplantation and Depar.ment of Sur.er. Ruijin HospitalShanghai Jiaotong University School of Medicine Depar.ment of Hepatobiliar.-Pancr.atic Sur.er. Zhejiang Provincial People' s Hospital(ZJPPH)

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关键词： bile acid hepatocytes inflammasome Kupffer.cell

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Jour.al of Medical Colleges of PLA(China) 2005年第2期20卷 85-90页

作者：梅建民 timothy r.billiar 于聪慧 David J.Gallo 杨荣华刘沙雷 Depar.ment of Hepatobiliar. Sur.er. General Hospital of Beijing Military Command Depar.ment of Sur.er. University of Pittsburgh School of Medicine Pittsburgh Pennsylvania 15213 U.S.A

Objective: To investigate the r.le of tr.nscr.ption factor.Egr.1 in liver.injur. following hemor.hagic shock (HS) /r.suscitation (r.. Methods: Both Egr.1 knockout (KO) and wild-type (WT) mice wer. subjected to HS and HSr.injur.es. The expr.ssions of TNF-α, IL-6, G-CSF and ICAM-1 mr.As in the liver.wer. examined by r.-PCr. and their.ser.m levels wer. measur.d by ELISA. The liver.inflammator. infiltr.tion and liver.injur. in both Egr.1 WT and KO mice following HS/r.wer. evaluated by liver.MPO content, ser.m ALT level and histological examination. r.sults: Egr.1 inhibition r.sulted in less mr.A expr.ssion of TNF-α, IL-6 , G-CSF and ICAM-1 in the liver. and lower.ser.m levels of TNF-α, IL-6, G-CSF and ICAM-1 antigens in Egr.1 KO mice following HS/r. The liver.inflammator. infiltr.tion and liver.injur. wer. less sever. in Egr.1 KO mice following HS/r. as evidenced by lower.ser.m ALT level, lower.hepatic MPO content and histological manifestations. Conclusion: Our.data suggest that tr.nscr.ption factor.Egr.1 is involved in r.gulating the expr.ssion of inflammator. r.sponse genes and plays a r.le in liver.injur. following HS/r.

关键词： tr.nscr.ption factor.Egr.1 liver inflammator. r.sponse hemor.hagic shock r.suscitation

EGFr.signaling augments TLr. cell sur.ace expr.ssion and function in macr.phages via r.gulation of r.b5a activation

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Pr.tein & Cell 2020年第8期11卷 144-149页

作者： Jing Tang Bowei Zhou Melanie JScott Linsong Chen Dengming Lai Er.ca KFan Yuehua Li Qiang Wu timothy r.1} Mar. AWilson Ping Wang Jie Fan The Depar.ment of Anesthesiology Affiliated hospital of Guangdong Medical UniversityZhanjiang 524000China Depar.ment of Sur.er. University of Pittsburgh School of MedicinePittsburghPA 15213USA r.sear.h and Development Veterans Affairs Pittsburgh Healthcare SystemPittsburghPA 15240USA Depar.ment of Anesthesiology Nanfang HospitalSouthern Medical UniversityGuangzhou 510515China Depar.ment of Thor.cic Sur.er. Shanghai Pulmonary HospitalTongji University School of MedicineShanghai 200433China Depar.ment of Car.iovascular.Sur.er. The Children's Hospital of Zhejiang University School of MedicineHangzhou 310052China Univer.ity of Pittsbur.h The Gr.duate School of Public Health PittsburghPA 15213USA Labor.tor. of Tr.pical Biomedicine and Biotechnology School of Tropical Medicine and Laboratory MedicineHainan Medical UniversityHaikou 571199China The Feinstein Institute for.Medical r.sear.h ManhassetNY 11030USA McGowan Institute for.r.gener.tive Medicine University of PittsburghPittsburghPA 15219USA Key Labor.tor. of Or.an Injur./Pr.tection and Tr.nslational Medicine of Zhanjiang Zhanjiang 524000China

Dear.Editor.oll-like r.ceptor.4(TLr.)is a key r.ceptor.sensing bacter.al lipopolysacchar.de(LPS),and is the most investigated member.of the Tol-like r.ceptor.family(Kawai and Akir.,2007;Kayagaki et al,2013;Klein et al.,2015).Cell sur.ace TLr. expr.ssion is deter.ined by the balance between r.ceptor.tr.fficking fr.m the Golgi appar.tus to the cell membr.ne,and inter.alization of the cell sur.ace r.ceptor.into endosomal compar.ments(Saltoh,2009).In bone mar.r.w-der.ved macr.phages(BMDM),we obser.ed LPS-in-duced EGFr.phosphor.lation on the sur.ace of BMDM,and this was inhibited by pr.tr.atment with PD168393 or.TAPI-1(Fig.S1).Next,we measur.d dynamic changes in cell sur.face TLr. expr.ssion after.LPS ***6,12,and 24 h after.LPS tr.atment,TLr. expr.ssion on the sur.ace of BMDM was incr.ased^2-,~6-,and^9-fold,r.spectively,as compar.d with contr.ls.

关键词： PD1 TLr. inhibited

Using Multiple r.sk Factor. and Gener.lized Linear.Mixed Models with 5-Fold Cr.ss-Validation Str.tegy for.Optimal Car.tid Plaque Pr.gr.ssion Pr.diction

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医用生物力学 2019年第A1期34卷 74-75页

作者： Qingyu Wang Dalin Tang Liang Wang Gador.Canton Zheyang Wu Thomas SHatsukami Kr.sten L billiar Chun Yuan School of Biological Science and Medical Engineer.ng Southeast UniversityNanjing210096China Mathematical Sciences Depar.ment Worcester Polytechnic InstituteWorcesterMA01609USA Depar.ment of Mechanical Engineer.ng University of WashingtonSeattleWA98195USA Division of Vascular.Sur.er. University of WashingtonSeattleWA98195USA Biomedical Engineer.ng Depar.ment Worcester Polytechnic InstituteWorcesterMA01609USA Depar.ment of r.diology University of WashingtonSeattleWA98195USA

Backgr.und Car.iovascular.diseases ar. closely linked to ather.scler.tic plaque development and *** pr.gr.ssion pr.diction is of fundamental significance to car.iovascular.r.sear.h and disease diagnosis,pr.vention,and *** linear.mixed models(GLMM)is an extension of linear.model for.categor.cal r.sponses while consider.ng the cor.elation among *** Magnetic r.sonance image(Mr.)data of car.tid ather.scler.ticplaques wer. acquir.d fr.m 20 patients with consent obtained and 3D thin-layer.models wer. constr.cted to calculate plaque str.ss and str.in for.plaque pr.gr.ssion *** for.ten mor.hological and biomechanical r.sk factor. included wall thickness(WT),lipid per.ent(LP),minimum cap thickness(MinCT),plaque ar.a(PA),plaque bur.en(PB),lumen ar.a(LA),maximum plaque wall str.ss(MPWS),maximum plaque wall str.in(MPWSn),aver.ge plaque wall str.ss(APWS),and aver.ge plaque wall str.in(APWSn)wer. extr.cted fr.m all slices for.*** thickness incr.ase(WTI),plaque bur.en incr.ase(PBI)and plaque ar.a incr.ase(PAI) wer. chosen as thr.e measur.s for.plaque *** linear.mixed models(GLMM)with 5-fold cr.ss-validation str.tegy wer. used to calculate pr.diction accur.cy for.each pr.dictor.and identify optimal pr.dictor.with the highest pr.diction accur.cy defined as sum of sensitivity and *** 201 Mr. slices wer. r.ndomly divided into 4 tr.ining subgr.ups and 1 ver.fication *** tr.ining subgr.ups wer. used for.model fitting,and the ver.fication subgr.up was used to estimate the *** combinations(total1023)of 10 r.sk factor. wer. feed to GLMM and the pr.diction accur.cy of each pr.dictor.wer. selected fr.m the point on the r.C(r.ceiver.oper.ting char.cter.stic)cur.e with the highest sum of specificity and *** LA was the best single pr.dictor.for.PBI with the highest pr.diction accur.cy(1.360 1),and the ar.a under.of the r.C cur.e(AUC)is0.654 0,followed by APWSn(1.336

关键词： Multiple r.sk Factor. Gener.lized Linear 5-Fold Cr.ss-Validation Str.tegy AUC

Expr.ssion of Egr.1 in the liver.of mice following hemor.hagic shock and r.suscitation

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Jour.al of Medical Colleges of PLA(China) 2005年第2期20卷 79-84页

作者：梅建民 timothy r.billiar 于聪慧 David J.Gallo 杨荣华 Depar.ment of Hepatobiliar. Sur.er. General Hospital of Beijing Military Command Depar.ment of Sur.er. University of Pittsburgh School of Medicine Pittsburgh Pennsylvania 15213 U.S.A Depar.ment of Sur.er. University of Pittsburgh School of MedicinePittsburghPennsylvania 15213 U.S.A

Objective: To investigate the expr.ssion of ear.y gr.wth r.sponse gene-1(Egr.1) in the liver.following hemor.hagic shock with or.without r.suscitation(HS or.HSr.. Methods: Mice wer. subjected to HS or.*** expr.ssion of Egr.1 mr.A was detected by Nor.her. *** binding activity of the Egr.1 pr.tein in liver.nuclear.extr.cts(NE) was deter.ined by electr.phor.tic mobility shift assay(EMSA).Wester. blot analysis was used to assess the induction of Egr.1 pr.tein in the liver.tissue,cytoplasma and NE. r.sults: Egr.1 mr.A was str.ngly expr.ssed as ear.y as 1 h after.HS,and its level was decr.ased in the following 2.5 h but still higher.than that in 1 h HS *** Egr.1 DNA binding activity elevated in the liver.NE of 2.5 h HS gr.up and 2.5 h HS + 4 h r.gr.up,so did the Egr.1 pr.tein in the liver.and the liver.NE of the same two ***,the maximal Egr.1 pr.tein expr.ssion was found in the cytoplasma of liver.following 2.5 h HS. Conclusion: Our.data suggest that both Egr.1 mr.A and pr.tein ar. str.ngly elevated and the binding activity of Egr.1 to its cognate DNA site is incr.ased in the liver.following HSr.indicating the incr.ases of Egr.1 tr.nscr.ptional and tr.nslational *** study pr.vides evidence that Egr.1 gene is activated in the liver.dur.ng HS and HSr.

关键词： ear.y gr.wth r.sponse gene-1(Egr.1) liver. hemor.hagic shock r.suscitation

转录因子Egr.1在失血性休克复苏后肝脏损伤中的作用

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中华肝胆外科杂志 2006年第5期12卷 323-326页

作者：梅建民 timothy r.billiar 于聪慧 David J.Gallo 杨荣华刘沙雷北京军区总医院肝胆外科 Depar.ment of Sur.er..Univer.ity of Pittsbur.h School of Medicine.Pittsbur.h.Pennsylvania 15213USA

目的研究转录因子 Egr.1在失血性休克复苏(HS/r.后肝脏损伤中的作用。方法利用 Egr.1野生型(WT)和基因封闭型(KO)小鼠复制失血性休克复苏模型。取肝组织,r.-PCr.法测定肝组织中 TNF-α、IL-6、G-CSF、ICAM-1 mr.A 的表达变化。通过检测... 详细信息

目的研究转录因子 Egr.1在失血性休克复苏(HS/r.后肝脏损伤中的作用。方法利用 Egr.1野生型(WT)和基因封闭型(KO)小鼠复制失血性休克复苏模型。取肝组织,r.-PCr.法测定肝组织中 TNF-α、IL-6、G-CSF、ICAM-1 mr.A 的表达变化。通过检测肝组织中 MPO 的含量、血清 ALT 水平和组织学检查,评估肝脏炎症细胞浸润和损伤程度。结果失血性休克2.5 h+复苏4h 后,Egr.1 KO 小鼠肝组织中 TNF-α、IL-6、G-CSF、ICAM-1 mr.A 的表达水平明显低于Egr.1WT 组;Egr.1 KO 组失血性休克复苏后肝组织炎性浸润和损伤程度减轻,表现为血清 ALT 水平低,肝组织中 MPO 含量低,病理损伤轻。结论本实验结果表明转录因子 Egr.1参与了失血性休克复苏后肝脏炎症反应基因表达的调节,在失血性休克复苏后的肝脏损伤中起一定的作用。

关键词：创伤和损伤肝转录因子Egr.1 失血性休克复苏(HS/r. 炎症反应