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kupffer cells contribute to concanavalin A-induced hepatic injury through a Th1 but not Th17 type response-dependent pathway in mice

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Hepatobiliary & Pancreatic Diseases International 2011年第2期10卷 171-178页

作者： Lin Chen,Xiao-Jun Xie,Yu-Fu Ye,Lin Zhou,Hai-Yang Xie,Qin-Fen Xie, Jiong Tian and Shu-Sen ZhengZhejiang University School of Medicine,Hangzhou 310003,ChinaKey Laboratory of Combined Multi-organ Transplantation,Ministry of Public Health Department of Hepatobiliary and Pancreatic Surgery Department of Nephrology,First Affiliated Hospital,Zhejiang University School of Medicine,Hangzhou 310003,China Zhejiang University School of Medicine Hangzhou 310003 China Key Laboratory of Combined Multi-organ Transplantation Ministry of Public Health Department of Hepatobiliary and Pancreatic Surgery First Affiliated Hospital Zhejiang University School of Medicine Hangzhou 310003 China Department of Nephrology First Affiliated Hospital Zhejiang University School of Medicine Hangzhou 310003 China

BACKGROUND:Increasing evidence suggests that a close interaction of kupffer cells with T cells plays a central role in concanavalin A-induced hepatic injury in mice,but the underlying mechanisms remain *** present study aimed to determine the relative roles of Th1 and Th17 type responses in concanavalin A-induced hepatic injury in mice, and to investigate whether or not kupffer cells contribute to hepatic injury via a Th1 or Th17 type response-dependent pathway. METHODS:Immune-mediated hepatic injury was induced in C57BL/6 mice by intravenous injection of concanavalin A. kupffer cells were inactivated by pretreatment with gadolinium chloride 24 hours before the concanavalin A *** interferon-gamma(IFN-γ)and interleukin-17(IL-17)pathways were blocked by specific neutralizing *** injury was assessed using serum transferase activity and pathological *** of inflammatory cytokines within the liver was detected by real-time polymerase chain reaction and immunohistochemistry. RESULTS:Neutralization of IFN-γsignificantly attenuated concanavalin A-induced hepatic ***,neutralization of IL-17 failed to suppress the *** of kupffer cells by gadolinium chloride pretreatment protected against concanavalin A-induced injury and significantly reduced hepatic cytokine levels including TNF-α,IL-6 and IFN-γbut not ***:Our findings suggest that kupffer cells contribute to concanavalin A-induced hepatic injury via a Th1 type response-dependent pathway and production of inflammatory cytokines including TNF-α,IL-6 and IFN-γ.

关键词： kupffer cells interferon-gamma interleukin-17 concanavalin A hepatic injury hepatitis

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Decreased phagocytic activity of kupffer cells in a rat nonalcoholic steatohepatitis model

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World Journal of Gastroenterology 2008年第39期14卷 6036-6043页

作者： Tatsuhiro Tsujimoto Hideto Kawaratani Toshiyuki Kitazawa Toshiko Hirai Hajime Ohishi Mitsuteru Kitade Hitoshi Yoshiji Masahito Uemura Hiroshi Fukui Third Department of Internal Medicine Nara Medical University840 Shijo-choKashiharaNara 634-8522Japan Department of Endoscopy and Ultrasound Nara Medical University840 Shijo-choKashiharaNara 634-8522Japan

AIM: To investigate kupffer cell dynamics and phagocytic activity,using a rat nonalcoholic steatohepatitis (NASH) model. METHODS: Male F344 rats were fed either a control diet or a choline-deficient L-amino acid-defined (CDAA) diet,followed by contrast enhanced ultrasonography (CEUS) using Levovist. The uptake of latex beads by the kupffer cells was determined by fluorescent microscopy. The status of the kupffer cells was compared between the two groups,using the immunohistochemical staining technique. RESULTS: After 4 or more wk of the CDAA diet,CEUS examination revealed a decrease in the signal intensity,20 min after intravenous Levovist. Fluorescent microscopic examination showed that the uptake of latex beads by the kupffer cells was reduced at week 1 and 2 in the study group,compared with the controls,with no further reduction after 3 wk. Immunohistochemical staining revealed no significant difference in the kupffer cell counts between the control group and the CDAA group. CONCLUSION: CEUS examination using Levovist demonstrated reduced contrast effect and phagocytic activity in the liver parenchymal phase,although the kupffer cell numbers were unchanged,indicating reduced phagocytic function of the kupffer cells in the rat NASH model. We believe that CEUS examination using Levovist is a useful screening modality,which can detect NASH in fatty liver patients.

关键词： Nonalcoholic steatohepatitis kupffer cells Contrast enhanced ultrasonography Levovist Ultrasound contrast agent Phagocytic activity

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Heme oxygenase-1 protects donor livers from ischemia/reperfusion injury:The role of kupffer cells

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World Journal of Gastroenterology 2010年第10期16卷 1285-1292页

作者： Zeng, Zhong Huang, Han-Fei Chen, Ming-Qing Song, Fei Zhang, Yu-Jun Kunming Med Coll Organ Transplantat Ctr Affiliated Hosp 1 Kunming 650032 Yunnan Province Peoples R China Third Mil Med Univ Southwest Hosp Inst Hepatobiliary Surg Chongqing 400038 Peoples R China

AIM:To examine whether heme oxygenase (HO)-1 overexpression would exert direct or indirect effects on kupffer cells activation, which lead to aggravation of reperfusion ***: Donors were pretreated with cobalt protoporphyrin (CoPP) or zinc protoporphyrin (ZnPP), HO-1 inducer and antagonist, respectively. Livers were stored at 4℃ for 24 h before transplantation. kupffer cells were isolated and cultured for 6 h after liver ***: Postoperatively, serum transaminases were significantly lower and associated with less liver injury when donors were pretreated with CoPP, as compared with the ZnPP group. Production of the cytokines tumor necrosis factor-α and interleukin-6 generated by kupffer cells decreased in the CoPP group. The CD14 expression levels (RT-PCR/Western blots) of kupffer cells from CoPP-pretreated liver grafts ***: The study suggests that the potential utility of HO-1 overexpression in preventing ischemia/reperfusion injury results from inhibition of kupffer cells activation.

关键词： Heme oxygenase-1 kupffer cells Ischemia/reperfusion injury Liver transplantation

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Prokineticin 2/Bv8 is expressed in kupffer cells in liver and is down regulated in human hepatocellular carcinoma

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World Journal of Gastroenterology 2008年第8期14卷 1182-1191页

作者： Justin Monnier Claire Piquet-Pellorce Jean-Jacques Feige Orlando Musso Bruno Clément Bruno Turlin Nathalie Théret Michel Samson INSERM U620 Université de Rennes 1 IFR140 2 avenue du Pr. Léon Bernard Rennes cedex 35043 France INSERM U522 Rennes France INSERM U878 Grenoble France Service d'Anatomo-pathologie CHU Pontchaillou Rennes France

AIM： TO study the implication of prokineticin 1 （PKI/EGVEGF） and prokineticin 2 （PK2/13v8） in hepatocellular carcinoma angiogenesis.METHODS： The gene induction of PK1/EG-VEGF and PK2/Bv8 was investigated in 10 normal, 28 fibrotic and 28 tumoral livers by using real time PCR. Their expression was compared to the expression of VEGF （an angiogenesis marker）, vWF （an endothelial cell marker） and to CD68 （a monocyte/macrophage marker）. Furthermore, the rnRNA levels of PK1/EG-VEGF, PK2/Bv8, prokineticin receptor 1 and 2 were evaluated by real time PCR in isolated liver cell populations. Finally, PK2/Bv8 protein was detected in normal liver paraffin sections and in isolated liver cells by immunohistochernistry and immunocytochemistry.RESULTS： PK2/Bv8 mRNA but not PK1/EG-VEGF was expressed in all types of normal liver samples examined. In the context of liver tumor development, we reported that PK2/13v8 correlates only with CD68 and showed a significant decrease in expression as the pathology evolves towards cancer. Whereas, VEGF and vWF mRNA were significantly upregulated in both fibrosis and HCC,as expected. In addition, out of all isolated liver cells examined, only kupffer cells （liver resident macrophages） express significant levels of PK2/Bv8 and its receptors, prokineticin receptor 1 and 2.CONCLUSION： In normal liver PK2/Bv8 and its receptors were specifically expressed by kupffer cells. PK2/Bv8 expression decreased as the liver evolves towards cancer and did not correlate with HCC angiogenesis.

关键词： Prokineticin Hepatocellular carcinoma PK2/Bv8 Angiogenesis kupffer cells Vascular endothelial growth factor Liver

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Laser capture microdissection and genetic analysis of carbon-labeled kupffer cells

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World Journal of Gastroenterology 2009年第14期15卷 1708-1718页

作者： Stephan Gehring Edmond Sabo Maryann E San Martin Elizabeth M Dickson Chao-Wen Cheng Stephen H Gregory Department of Medicine Rhode Island Hospital and The Warren Alpert Medical School of Brown University Providence RI 02903 United States Department of Pathology Rhode Island Hospital and The Warren Alpert Medical School of Brown University Providence RI 02903 United States zentrum fur Kinder- und Jugendmedizin der Universitaitsmedizin der Johannes Gutenberg-Universitait 55101 Mainz Germany

AIM： To develop a method of labeling and microdissecting mouse kupffer cells within an extraordinarily short period of time using laser capture microdissection （LCM）. METHODS： Tissues are complex structures comprised of a heterogeneous population of interconnected cells. LCM offers a method of isolating a single cell type from specific regions of a tissue section. LCM is an essential approach used in conjunction with molecular analysis to study the functional interaction of cells in their native tissue environment. The process of labeling and acquiring cells by LCM prior to mRNA isolation can be elaborate, thereby subjecting the RNA to considerable degradation. kupffer cell labeling is achieved by injecting India ink intravenously, thus circumventing the need for in vitro staining. The significance of this novel approach was validated using a cholestatic liver injury model. RESULTS： mRNA extracted from the microdissected cell population displayed marked increases in colonystimulating factor-1 receptor and kupffer cell receptor message expression, which demonstrated kupffer cell enrichment. Gene expression by kupffer ceils derived from bile-duct-ligated, versus sham-operated, mice was compared. Microarray analysis revealed a significant （2.5-fold, q value 〈 10） change in 493 genes. Based on this fold-change and a standardized PubMed search, 10 genes were identified that were relevant to the ability of kupffer cells to suppress liver injury. CONCLUSION; The methodology outlined herein provides an approach to isolating high quality RNA from kupffer cells, without altering the tissue integrity.

关键词： kupffer cells India ink Laser capturemicrodissection Bile duct ligation DNA microarray

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Production of reactive oxygen species and expression of inducible nitric oxide synthase in rat isolated kupffer cells stimulated by Leptospira interrogans and Borrelia burgdorfen

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World Journal of Gastroenterology 2006年第19期12卷 3077-3081页

作者： Antonella Marangoni Silvia Accardo Rita Aldini Massimo Guardigli Francesca Cavrini Vittorio Sambri Marco Montagnani Aldo Roda Roberto Cevenini Sezione di Microbiologia DMCSS University of Bologna BolognaItaly Istituto di Scienze Chimiche University of Bologna BolognaItaly Dipartimento di Scienze Farmaceutiche University of Bologna BolognaItaly Dipartimento di Medicina Interna e Gastroenterologia University of Bologna BolognaItaly

AIM： To evaluate the production of reactive oxygen species （ROS） and the expression of inducible nitric oxide synthase （iNOS） in rat isolated kupffer cells （KCs） stimulated by Leptospira interrogans and Borrelia burgdorferi. METHODS： Rat kupffer cells were separated by perfusion of the liver with 0.05% collagenase, and purified by Percoll gradients. Pudfied kupffer cells were tested in vitro with alive *** and B. burgdorferi preparations. The production of ROS was determined by chemiluminescence, whereas iNOS protein expression was evaluated by Western blot assay using anti-iNOS antibodies. RESULTS： B. burgdorferi and to a less extent L. interrogans induced ROS production with a peak 35 min after infection. The chemiluminescence signal progressively diminished and was undetectable by 180 min of incubation. Leptospirae and borreliae induced an increased iNOS expression in kupffer cells that peaked at 6 hours and was still evident 22 h after infection. CONCLUSION： Both genera of spirochetes induced ROS and iNOS production in rat kupffer cells. Since the cause of liver damage both in leptospiral as well as in borrelial infections are still unknown, we suggest that leptospira and borrelia damage of the liver can be initially mediated by oxygen radicals, and is then maintained at least in part by nitric oxide.

关键词： Leptospira interrogans Borrelia burgdorferi Inducible nitric oxide synthase Nitric oxide Reactive oxygen species kupffer cells Chemiluminescence

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Synthesis of platelet-activating factor and its receptor expression in kupffer cells in rat carbon tetrachloride-induced cirrhosis

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World Journal of Gastroenterology 2008年第5期14卷 764-770页

作者： Yin-Ying Lu Chun-Ping Wang Lin Zhou Yan Chen Shu-Hui Su Yong-Yi Feng Yong-Ping Yang Department of Gastroenterology 302 Hospital of Chinese PLA Beijing 100039 China

AIM:To determine the platelet-activating factor (PAF) synthesis and its receptor expression in kupffer cells in rat carbon tetrachloride-induced cirrhosis. METHODS:kupffer cells, isolated from the livers of control and CCl4-induced cirrhotic rats, were placed in serum-free medium overnight. PAF saturation binding, ET-1 saturation and competition binding were assayed. ET-1 induced PAF synthesis, mRNA expression of PAF, preproendothelin-1, endothelin A (ETA) and endothelin B (ETB) receptors were also determined. RESULTS:A two-fold increase of PAF synthesis (1.42 ± 0.14 vs 0.66 ± 0.04 pg/μg DNA) and a 1.48-fold increase of membrane-bound PAF (1.02 ± 0.06 vs 0.69 ± 0.07 pg/μg DNA) were observed in activated kupffer cells of cirrhotic rats. The application of ET-1 to kupffer cells induced PAF synthesis in a concentration-dependent manner in both cirrhotic and normal rats via ETB receptor, but PAF synthesis in the activated kupffer cells was more effective than that in the normal kupffer cells. In activated kupffer cells, PAF receptor expression and PAF binding capacity were markedly enhanced. Activated kupffer cells raised the [125I]-ET-1 binding capacity, but changed neither the affinity of the receptors, nor the expression of ETA receptor. CONCLUSION:kupffer cells in the course of CCl4-induced cirrhosis are the main source of increased PAF. ET-1 is involved endogenously in stimulating the PAF synthesis in activated kupffer cells via ETB receptor by paracrine. ETA receptor did not appear in activated kupffer cells, which may exacerbate the hepatic and extrahepatic complications of cirrhosis.

关键词： Platelet activating factor kupffer cells Receptor Cirrhosis

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Heme oxygenase 1-mediated ferroptosis in kupffer cells initiates liver injury during heat stroke

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Acta Pharmaceutica Sinica B 2024年第9期14卷 3983-4000页

作者： Ru Li Riqing Wei Chenxin Liu Keying Zhang Sixiao He Zhifeng Liu Junhao Huang Youyong Tang Qiyuan An Ligen Lin Lishe Gan Liying Zhao Xiaoming Zou Fudi Wang Yuan Ping Qiang Ma The Seventh Affiliated Hospital Southern Medical UniversityFoshan 528244China Department of Biopharmaceutics School of Laboratory Medicine and BiotechnologySouthern Medical UniversityGuangzhou 510000China Medical Critical Care Medicine General Hospital of Southern Theatre Command of PLAGuangzhou 510000China Guangdong Branch Center National Clinical Research Center for Geriatric Diseases(Chinese PLA General Hospital)Guangzhou 510000China State Key Laboratory of Quality Research in Chinese Medicine Institute of Chinese Medical SciencesUniversity of MacaoAvenida da UniversidadeTaip1Macao 999078China School of Pharmaceutical Sciences Zhejiang Chinese Medical UniversityHangzhou 311402China Department of General Surgery Nanfang Hospitalthe First School of Clinical MedicineSouthern Medical UniversityGuangzhou 510000China The Fourth Affiliated Hospital the First Affiliated HospitalSchool of Public HealthInstitute of Translational MedicineCancer CenterState Key Laboratory of Experimental HematologyZhejiang University School of MedicineHangzhou 310000China The First Affiliated Hospital the Second Affiliated HospitalBasic Medical SciencesSchool of Public HealthHengyang Medical SchoolUniversity of South ChinaHengyang 421200China College of Pharmaceutical Sciences Zhejiang UniversityHangzhou 310000China Liangzhu Laboratory Zhejiang University Medical CenterHangzhou 310000China Guangdong Provincial Key Laboratory of Immune Regulation and Immunotherapy School of Laboratory Medicine and BiotechnologySouthern Medical UniversityGuangzhou 510000China

With the escalating prevalence of global heat waves,heat stroke has become a prominent health concern,leading to substantial liver *** other forms of liver injury,heat strokeinduced damage is characterized by heat cytotoxicity and heightened inflammation,directly contributing to elevated mortality *** clinical assessments have identified elevated bilirubin levels as indicative of kupffer cell dysfunction,their specific correlation with heat stroke liver injury remains *** hypothesis proposes the involvement of kupffer cell ferroptosis during heat stroke,initiating IL-1bmediated *** single-cell RNA sequencing of murine macrophages,a distinct and highly susceptible kupffer cell subtype,Clec4Ft/CD206t,emerged,with heme oxygenase 1(HMOX-1)playing a pivotal ***,heat-induced HMOX-1,regulated by early growth response factor 1,mediated ferroptosis in kupffer cells,specifically in the Clec4F t/CD206 t subtype(KC2),activating phosphatidylinositol 4-kinase beta and promoting PI4P *** cascade triggered NLRP3 inflammasome activation and maturation of *** findings underscore the critical role of targeted therapy against HMOX-1 in ferroptosis within kupffer cells,particularly in Clec4F t/CD206 t *** an approach has the potential to mitigate inflammation and alleviate acute liver injury in the context of heat stroke,offering a promising avenue for future therapeutic interventions.

关键词： Heat stroke Liver injury kupffer cells Ferroptosis Heme oxygenase 1 Phosphatidylinositol 4-kinase beta NLRP3 Early growth response factor 1

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Chlamydia pneumoniae replicates in kupffer cells in mouse model of liver infection

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World Journal of Gastroenterology 2006年第40期12卷 6453-6457页

作者： Antonella Marangoni Manuela Donati Francesca Cavrini Rita Aldini Silvia Accardo Vittorio Sambri Marco Montagnani Roberto Cevenini Sezione di Microbiologia DMCSS University of Bologna Bologna Italy Dipartimento SMETC University of Bologna Bologna Italy Dipartimento di Medicina Interna e Gastroenterologia University of Bologna Bologna Italy

AIM: To develop an animal model of liver infection with Chlamydia pneumoniae (C. pneumoniae) in intraperito-neally infected mice for studying the presence of chlamy-diae in kupffer cells and ***: A total of 80 BALB/c mice were inoculated intraperitoneally with C. pneumoniae and sacrificed at various time points after infection. Chlamydiae were looked for in liver homogenates as well as in kupffer cells and hepatocytes separated by liver perfusion with collagenase. C. pneumoniae was detected by both isola-tion in LLC-MK2 cells and fluorescence in situ hybridiza-tion (FISH). The releasing of TNFA-α by C. pneumoniae in vitro stimulated kupffer cells was studied by enzyme-linked immunosorbent ***: C. pneumoniae isolation from liver homoge-nates reached a plateau on d 7 after infection when 6 of 10 animals were positive, then decreased, and became negative by d 20. C. pneumoniae isolation from sepa-rated kupffer cells reached a plateau on d 7 when 5 of 10 animals were positive, and became negative by d 20. The detection of C. pneumoniae in separated kupffer cells by FISH, confirmed the results obtained by culture. Isolated hepatocytes were always negative. Stimula-tion of kupffer cells by alive C. pneumoniae elicited high TNF-α levels. CONCLUSION: A productive infection by C. pneumo-niae may take place in kupffer cells and C. pneumoniae induces a local pro-inflammatory activity. C. pneumoniae is therefore, able to act as antigenic stimulus when local-ized in the liver. One could speculate that C. pneumoniaeinfection, involving cells of the innate immunity such as kupffer cells, could also trigger pathological immune re-actions involving the liver, as observed in human patients with primary biliary cirrhosis.

关键词： Chlamydia pneumoniae Liver infection kupffer cells Hepatocytes Culture-isolation Fluorescence in situ hybridization TNF-α Primary biliary cirrhosis

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Xuebijing injection alleviates liver injury by inhibiting secretory function of kupffer cells in heat stroke rats

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Journal of Traditional Chinese Medicine 2013年第2期33卷 243-249页

作者： Yi Chen Huasheng Tong Xingqin Zhang Liqun Tang Zhiguo Pan Zhifeng Liu Pengkai Duan Lei Su Guangzhou University of Chinese Medicine Department of ICU General Hospital of Guangzhou Military CommandKey Laboratory of Tropical Zone Trauma Care andTissue Repair of PLA

OBJECTIVE： To evaluate the effects of Xuebijing （XBJ） injection in heat stroke （HS） rats and to inves- tigate the mechanisms underlying these effects. METHODS： Sixty anesthetized rats were random- ized into three groups and intravenously injected twice daily for 3 days with 4 mL XBJ （XBJ group） or phosphate buffered saline （HS and Sham groups） per kg body weight. HS was initiated in the HS and XBJ groups by placing rats in a simulated climate chamber （ambient temperature 40℃：, humidity 60% ）. Rectal temperature, aterial pressure, and heart rate were monitored and recorded. Time to HS onset and survival were determined, and serum concentrations of tumor necrosis factor （TNF）-α, in-terleukin （IL）-1β, IL-6, alanine-aminotransferase （ALT）, and aspartate-aminotransferase （AST） were measured. Hepatic tissue was harvested for patho- logical examination and electron microscopic ex- amination. kupffer cells （KCs） were separated from liver at HS initiation, and the concentrations of se- creted TNF-α, IL-1β3 and IL-6 were measured. RESULTS： Time to HS onset and survival were signif- icantly longer in the XBJ than in the HS group. Moreover, the concentrations of TNF-α, IL-1β, IL-6, ALT and AST were lower and liver injury was milder in the XBJ than in the HS group. Heat-stress in- duced structural changes in KCs and hepatic cells were more severe in the HS than in the XBJ group and the concentrations of TNF-α, IL-1β and IL-6 se- creted by KCs were lower in the XBJ than in the HS group. CONCLUSION： XBJ can alleviate HS-induced sys- temic inflammatory response syndrome and liver injury in rats, and improve outcomes. These protec- tive effects may be due to the ability of XBJ to inhib- it cytokine secretion by KCs.

关键词： Heat stroke kupffer cells Systemic in-flammatory response syndrome Xuebijing Liver in-jury Inflammatory cytokines

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