TNF-alpha but not IL-1alpha are Correlated with PGE<sub>1</sub>-Dependent Protection Against Acute D-Galactosamine-Induced Liver Injury

Muntané, Jordi; Montero, JL; Jm, Lozano; Miranda‐Vizuete, Antonio; Mata, Manuel de la; Míño, G

doi:10.1155/2000/416705

Cited by 17 publications

(18 citation statements)

References 25 publications

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“…Moreover, activated T cells can secrete many cytokines that may induce inflammation that exacerbate liver injury [34,35]. We examined the activation state of the T cells using CD69 as an activation marker by flow cytometry ( Fig.…”

Section: Secreted Il-1α Promotes T-cell Activationmentioning

confidence: 99%

Secreted IL‐1α promotes T‐cell activation and expansion of CD11b⁺Gr1⁺ cells in carbon tetrachloride‐induced liver injury in mice

et al. 2015

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Interleukin-1α is mainly expressed on the cell membrane, but can also be secreted during inflammation. The roles of secreted and membrane IL-1α in acute liver inflammation are still not known. Here, we examined the functions of secreted and membrane IL-1α in a mouse model of carbon tetrachloride-induced acute liver injury. We show that secreted IL-1α aggravates liver damage and membrane IL-1α slightly protects mice from liver injury. Further studies showed that secreted IL-1α promotes T-cell activation. It also increased the expansion of CD11b + Gr1 + myeloid cells, which may serve as a negative regulator of acute liver inflammation. Moreover, secreted IL-1α induced IL-6 production from hepatocytes. IL-6 neutralization reduced the proliferation of CD11b + Gr1 + myeloid cells in vivo. CCL2 and CXCL5 expression was increased by secreted IL-1α in vitro and in vivo. Antagonists of the chemokine receptors for CCL2 and CXCL5 significantly reduced the migration of CD11b + Gr1 + myeloid cells. These results demonstrate that secreted and membrane IL-1α play different roles in acute liver injury. Secreted IL-1α could promote Tcell activation and the recruitment and expansion of CD11b + Gr1 + myeloid cells through induction of CCL2, CXCL5, and IL-6. The controlled release of IL-1α could be a critical regulator during acute liver inflammation.Keywords: Acute liver injury r CD11b + Gr1 + myeloid cells r Membrane IL-1α r Secreted IL-1α r T-cell activation Additional supporting information may be found in the online version of this article at the publisher's web-site Correspondence: Dr. Haiyan Liu e-mail: hliu@suda.edu.cn IntroductionThe liver plays a central role in metabolic homeostasis [1]. Liver injury is mainly caused by various insults such as drug, chemical agents, viral hepatitis (hepatitis B or C viruses), alcohol, and C 2015 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim www.eji-journal.eu Eur. J. Immunol. 2015. 45: 2084-2098 Molecular immunology 2085 autoimmune attack of hepatocytes [2]. Liver damage by proinflammatory cytokines induced by these causes is a relevant mechanism for liver cell death [3]. Acute liver injury remains one of the most challenging problems in liver diseases, and new therapeutic options for treatment of acute liver injury are urgently needed [4]. Carbon tetrachloride (CCl 4 ) is widely used as a chemical inducer of acute or chronic liver injury in rodents depending on the dosage and administration frequency [5]. ROS and oxidative stress are then generated and inflammatory cells are recruited, which leads to hepatocyte degeneration and necrosis [6,7]. Parenchymal cells could regenerate that involves a complex regulated response after CCl 4 -induced acute liver injury [8]. Therefore, anti-oxidative and anti-inflammatory therapies are thought to be the effective ways to prevent and attenuate CCl 4 -induced liver damage. IL-1 is a pleiotropic cytokine and affects inflammatory immune responses. The IL-1 family includes two important agonistic proteins, IL-1α and IL-1β, which play an important role in ...

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Section: Secreted Il-1α Promotes T-cell Activationmentioning

confidence: 99%

Secreted IL‐1α promotes T‐cell activation and expansion of CD11b⁺Gr1⁺ cells in carbon tetrachloride‐induced liver injury in mice

et al. 2015

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“…Because TNF-␣ was suggested to mediate the development of GalN-hepatitis (6, 7) and Wallach et al (27) reported that preceding administration of TNF-␣ caused desensitization of mice to a lethal amount of TNF-␣, it would be likely that CBH desensitized the rats against GalN in the present study. The concentration of UDP-galactosamine in the liver of the rats increased rapidly after the injection of GalN (7)(8)(9)(10), and since the increase was accompanied by a reduction in the concentration of UTP and UDP-glucose in the liver, it is likely that the hepatotoxic action of GalN is mediated by suppression of RNA or glycoprotein biosynthesis caused by the deficiency of UTP or related compounds. Bauer et al (28) have reported inhibition of overall protein and glycoprotein secretion by GalN, and that was partially explained by inhibition of de novo protein synthesis.…”

Section: Discussionmentioning

confidence: 99%

“…Some investigators have indicated that an increase in blood endotoxin concentration after injection of GalN causes hepatic injury associated with secretion of cytokines, such as TNF-␣ and IL-6 from Kupffer cells ( 6,7 ). Endotoxin is a constituent of the cell wall of gram-negative bacteria, and since it may be absorbed from the gastrointestinal tract into the portal venous circulation, the intestinal microflora have generally been considered to be important for the development of GalN-hepatitis.…”

mentioning

confidence: 99%

Effects of Dietary Corn Bran Hemicellulose and Neomycin on Hepatic Caspase-3 Activity and Glycoprotein Concentration in Rats Treated with or without D-Galactosamine

Daizo

Egashira

Sanada

2006

J Nutr Sci Vitaminol

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SummaryThe effects of dietary corn bran hemicellulose (CBH) and neomycin (Neo) on hepatic caspase-3 activity and glycoprotein concentration were investigated to explore the possible mechanism of the alleviative action of dietary CBH and Neo on the development of D -galactosamine (GalN)-hepatitis. Rats were fed a diet containing 5% CBH with or without neomycin (Neo) for 7 or 14 d. On the last day of feeding, the rats were treated with GalN (400 mg/kg body weight, i.p.), and their plasma transaminase activities, hepatic glycoprotein concentrations and hepatic caspase-3 activities were determined 6 or 24 h later. Although the elevations of plasma transaminase activities were suppressed by CBH or Neo 24 h after GalN-treatment, the activities were not affected by CBH or Neo at an early stage (6 h) of GalN action. At 6 h, hepatic caspase-3 activity was elevated by CBH diet alone as high as that of the GalN-injected control-diet group, and the activity was not elevated further by GalN. At the same time, both GalN-treatment and CBH feeding reduced the hepatic glycoprotein (Mw. 64,000-74,000) concentration, but Neo did not affect the caspase activity or the glycoprotein concentration. These results suggest that dietary CBH elevates hepatic caspase-3 activity and reduces hepatic glycoprotein concentration, and may imply that CBH would suppress GalN-hepatitis not at the early-or middle-step of apoptosis but at the late-step of apoptosis or necrosis, although the relation between these phenomena and the alleviative effects of CBH and Neo on GalN-induced hepatitis is yet to be clarified.

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“…Los niveles séricos de óxido nítrico se determinaron indirectamente mediante la cuantificación de sus productos finales nitrito y nitrato (13). En el ensayo el nitrato se convirtió a nitrito mediante la nitrato reductasa y el nitrito total se determinó mediante la reacción de Griess.…”

Section: Determinación De Los Niveles De óXido Nítrico Glutatión Y Munclassified

Factores pronósticos de complicaciones postoperatorias en el trasplante hepático

Rodríguez‐Ariza¹,

Monrobel

Martı́nez-Galisteo³

et al. 2008

Rev. esp. enferm. dig.

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INTRODUCCIÓNEl trasplante hepático ortotópico (THO) es el tratamiento de elección para enfermedades hepáticas agudas o crónicas en estadio final. Sin embargo, el seguimiento de Factores pronósticos de complicaciones postoperatorias en el trasplante hepáticoA. Rodríguez-Ariza, A. Monrobel, E. Martínez-Galisteo 1 , C. Alicia Padilla 1 , J. A. Bárcena 1 , E. Fraga, G. Costán, P. Barrera, A. Poyato, J. L. Montero, P. López-Cillero 2 , J. Muntané y M. de la Mata RESUMENObjetivo: la evolución postoperatoria de los pacientes sometidos a trasplante hepático ortotópico (THO) se encuentra frecuentemente asociada a la aparición de diversas complicaciones tales como disfunción renal, rechazo agudo, infecciones y complicaciones neurológicas. Estas complicaciones constituyen las causas más significativas de morbilidad y mortalidad tempranas en pacientes que reciben un THO. El propósito del presente estudio es la identificación de factores relacionados con las distintas complicaciones postoperatorias del THO. Diseño experimental: se llevó a cabo un estudio prospectivo.Pacientes: se analizaron 78 variables en 32 pacientes consecutivos sometidos a THO. Utilizando un análisis de regresión logística se identificaron aquellos factores asociados de forma independiente con la aparición de complicaciones postoperatorias.Resultados: el análisis multivariante demostró que los niveles pretrasplante en suero de malondialdehído y creatinina estaban asociados con el desarrollo de disfunción renal. Los niveles pretrasplante de hemoglobina y las unidades de plaquetas administradas durante la cirugía fueron factores pronósticos de infecciones. El rechazo agudo fue pronosticado por los niveles séricos de γ-glutamil transpeptidasa y de bilirrubina total. Los niveles pretrasplante de sodio y glutaredoxina en suero estuvieron asociados con complicaciones neurológicas.Conclusiones: proponemos estos marcadores para la identificación de pacientes de alto riesgo, permitiendo una vigilancia y/o tratamiento anticipados que mejorarán la morbilidad y la supervivencia en pacientes sometidos a THO. ABSTRACTObjectives: the postoperative evolution of patients submitted to orthotopic liver transplant (OLT) is frequently associated with the appearance of different types of complications such as renal failure, graft rejection, infections, and neurological disorders. These complications are the most significant causes of early morbidity and mortality in patients undergoing OLT. The purpose of the present study was the identification of factors related to the different postoperative complications after OLT. Experimental design: a prospective study was carried out.Patients: seventy-eight variables were analyzed in 32 consecutive patients undergoing OLT. The factors independently associated with the appearance of postoperative complications were identified using a stepwise logistic regression analysis.Results: the multivariate analysis showed that malondialdehyde and creatinine pretransplant serum levels were associated with the development of renal dysfunction. T...

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TNF-alpha but not IL-1alpha are Correlated with PGE₁-Dependent Protection Against Acute D-Galactosamine-Induced Liver Injury

Cited by 17 publications

References 25 publications

Secreted IL‐1α promotes T‐cell activation and expansion of CD11b⁺Gr1⁺ cells in carbon tetrachloride‐induced liver injury in mice

Secreted IL‐1α promotes T‐cell activation and expansion of CD11b⁺Gr1⁺ cells in carbon tetrachloride‐induced liver injury in mice

Effects of Dietary Corn Bran Hemicellulose and Neomycin on Hepatic Caspase-3 Activity and Glycoprotein Concentration in Rats Treated with or without D-Galactosamine

Factores pronósticos de complicaciones postoperatorias en el trasplante hepático

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TNF-alpha but not IL-1alpha are Correlated with PGE1-Dependent Protection Against Acute D-Galactosamine-Induced Liver Injury

Cited by 17 publications

References 25 publications

Secreted IL‐1α promotes T‐cell activation and expansion of CD11b+Gr1+ cells in carbon tetrachloride‐induced liver injury in mice

Secreted IL‐1α promotes T‐cell activation and expansion of CD11b+Gr1+ cells in carbon tetrachloride‐induced liver injury in mice

Effects of Dietary Corn Bran Hemicellulose and Neomycin on Hepatic Caspase-3 Activity and Glycoprotein Concentration in Rats Treated with or without D-Galactosamine

Factores pronósticos de complicaciones postoperatorias en el trasplante hepático

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TNF-alpha but not IL-1alpha are Correlated with PGE₁-Dependent Protection Against Acute D-Galactosamine-Induced Liver Injury

Secreted IL‐1α promotes T‐cell activation and expansion of CD11b⁺Gr1⁺ cells in carbon tetrachloride‐induced liver injury in mice

Secreted IL‐1α promotes T‐cell activation and expansion of CD11b⁺Gr1⁺ cells in carbon tetrachloride‐induced liver injury in mice