Low-molecular-weight hyaluronic acid induces nuclear factor-kappaB-dependent resistance against tumor necrosis factor alpha-mediated liver injury in mice.

D Wolf; J Schümann; K Koerber; A K Kiemer; A M Vollmar; G Sass; T Papadopoulos; R Bang; S D Klein; B Brüne; Gisa Tiegs

Low-molecular-weight hyaluronic acid induces nuclear factor-kappaB-dependent resistance against tumor necrosis factor alpha-mediated liver injury in mice.

Standard

Low-molecular-weight hyaluronic acid induces nuclear factor-kappaB-dependent resistance against tumor necrosis factor alpha-mediated liver injury in mice. / Wolf, D; Schümann, J; Koerber, K; Kiemer, A K; Vollmar, A M; Sass, G; Papadopoulos, T; Bang, R; Klein, S D; Brüne, B; Tiegs, Gisa.

in: HEPATOLOGY, Jahrgang 34, Nr. 3, 3, 2001, S. 535-547.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Wolf, D, Schümann, J, Koerber, K, Kiemer, AK, Vollmar, AM, Sass, G, Papadopoulos, T, Bang, R, Klein, SD, Brüne, B & Tiegs, G 2001, 'Low-molecular-weight hyaluronic acid induces nuclear factor-kappaB-dependent resistance against tumor necrosis factor alpha-mediated liver injury in mice.', HEPATOLOGY, Jg. 34, Nr. 3, 3, S. 535-547. <http://www.ncbi.nlm.nih.gov/pubmed/11526540?dopt=Citation>

APA

Wolf, D., Schümann, J., Koerber, K., Kiemer, A. K., Vollmar, A. M., Sass, G., Papadopoulos, T., Bang, R., Klein, S. D., Brüne, B., & Tiegs, G. (2001). Low-molecular-weight hyaluronic acid induces nuclear factor-kappaB-dependent resistance against tumor necrosis factor alpha-mediated liver injury in mice. HEPATOLOGY, 34(3), 535-547. [3]. http://www.ncbi.nlm.nih.gov/pubmed/11526540?dopt=Citation

Vancouver

Wolf D, Schümann J, Koerber K, Kiemer AK, Vollmar AM, Sass G et al. Low-molecular-weight hyaluronic acid induces nuclear factor-kappaB-dependent resistance against tumor necrosis factor alpha-mediated liver injury in mice. HEPATOLOGY. 2001;34(3):535-547. 3.

Bibtex

@article{b65d900287ff4ee5b7de0d6969f9ed6d,

title = "Low-molecular-weight hyaluronic acid induces nuclear factor-kappaB-dependent resistance against tumor necrosis factor alpha-mediated liver injury in mice.",

abstract = "Liver resident NK1.1+ T cells are supposed to play a pivotal role in the onset of inflammatory liver injury in experimental mouse models such as concanavalin A (Con A)-induced hepatitis. These cells, expressing the adhesion receptor, CD44, are largely depleted from the liver by a single intravenous injection of low-molecular-weight fragments of hyaluronic acid (LMW-HA). Here, we report that LMW-HA pretreatment protected mice from liver injury in several models of T-cell- and macrophage-dependent, tumor necrosis factor alpha (TNF-alpha)-mediated inflammatory liver injury, i.e., from liver injury induced by either Con A or Pseudomonas exotoxin A (PEA) or PEA/lipopolysaccharide (LPS). Interestingly, apart from inhibition of cellular adhesion, pretreatment of mice with LMW-HA was also capable of preventing hepatocellular apoptosis and activation of caspase-3 induced by direct administration of recombinant murine (rmu) TNF-alpha to D-galactosamine (GalN)-sensitized mice. LMW-HA-induced hepatoprotection could be neutralized by pretreatment with the nuclear factor-kappaB (NF-kappaB) inhibitor, pyrrolidine dithiocarbamate (PDTC), demonstrating the involvement of NF-kappaB in the observed protective mechanism. Indeed, injection of LMW-HA rapidly induced the production of TNF-alpha by Kupffer cells and the translocation of NF-kappaB into hepatocellular nuclei. Both LMW-HA-induced TNF-alpha production and NF-kappaB translocation were blocked by pretreatment with PDTC. Our findings provide evidence for an unknown mechanism of LMW-HA-dependent protection from inflammatory liver disease, i.e., induction of TNF-alpha- and NF-kappaB-dependent cytoprotective proteins within the target parenchymal liver cells.",

keywords = "Animals, Male, Mice, Mice, Inbred BALB C, CD4 Lymphocyte Count, Molecular Weight, Lymphocyte Count, Concanavalin A/pharmacology, Lipopolysaccharides/pharmacology, *ADP Ribose Transferases, Antigens, CD44/analysis, *Bacterial Toxins, Cell Death/drug effects, Cytokines/blood, Drug-Induced Liver Injury/pathology/*prevention & control, Exotoxins/pharmacology, Hyaluronic Acid/*chemistry/*pharmacology, Kupffer Cells/metabolism, Liver/pathology, Liver Failure/etiology/prevention & control, Macrophages/physiology, NF-kappa B/antagonists & inhibitors/*physiology, T-Lymphocytes/immunology/pathology/physiology, *Tumor Necrosis Factor-alpha, *Virulence Factors, Animals, Male, Mice, Mice, Inbred BALB C, CD4 Lymphocyte Count, Molecular Weight, Lymphocyte Count, Concanavalin A/pharmacology, Lipopolysaccharides/pharmacology, *ADP Ribose Transferases, Antigens, CD44/analysis, *Bacterial Toxins, Cell Death/drug effects, Cytokines/blood, Drug-Induced Liver Injury/pathology/*prevention & control, Exotoxins/pharmacology, Hyaluronic Acid/*chemistry/*pharmacology, Kupffer Cells/metabolism, Liver/pathology, Liver Failure/etiology/prevention & control, Macrophages/physiology, NF-kappa B/antagonists & inhibitors/*physiology, T-Lymphocytes/immunology/pathology/physiology, *Tumor Necrosis Factor-alpha, *Virulence Factors",

author = "D Wolf and J Sch{\"u}mann and K Koerber and Kiemer, {A K} and Vollmar, {A M} and G Sass and T Papadopoulos and R Bang and Klein, {S D} and B Br{\"u}ne and Gisa Tiegs",

year = "2001",

language = "English",

volume = "34",

pages = "535--547",

journal = "HEPATOLOGY",

issn = "0270-9139",

publisher = "John Wiley and Sons Ltd",

number = "3",

}

RIS

TY - JOUR

T1 - Low-molecular-weight hyaluronic acid induces nuclear factor-kappaB-dependent resistance against tumor necrosis factor alpha-mediated liver injury in mice.

AU - Wolf, D

AU - Schümann, J

AU - Koerber, K

AU - Kiemer, A K

AU - Vollmar, A M

AU - Sass, G

AU - Papadopoulos, T

AU - Bang, R

AU - Klein, S D

AU - Brüne, B

AU - Tiegs, Gisa

PY - 2001

Y1 - 2001

N2 - Liver resident NK1.1+ T cells are supposed to play a pivotal role in the onset of inflammatory liver injury in experimental mouse models such as concanavalin A (Con A)-induced hepatitis. These cells, expressing the adhesion receptor, CD44, are largely depleted from the liver by a single intravenous injection of low-molecular-weight fragments of hyaluronic acid (LMW-HA). Here, we report that LMW-HA pretreatment protected mice from liver injury in several models of T-cell- and macrophage-dependent, tumor necrosis factor alpha (TNF-alpha)-mediated inflammatory liver injury, i.e., from liver injury induced by either Con A or Pseudomonas exotoxin A (PEA) or PEA/lipopolysaccharide (LPS). Interestingly, apart from inhibition of cellular adhesion, pretreatment of mice with LMW-HA was also capable of preventing hepatocellular apoptosis and activation of caspase-3 induced by direct administration of recombinant murine (rmu) TNF-alpha to D-galactosamine (GalN)-sensitized mice. LMW-HA-induced hepatoprotection could be neutralized by pretreatment with the nuclear factor-kappaB (NF-kappaB) inhibitor, pyrrolidine dithiocarbamate (PDTC), demonstrating the involvement of NF-kappaB in the observed protective mechanism. Indeed, injection of LMW-HA rapidly induced the production of TNF-alpha by Kupffer cells and the translocation of NF-kappaB into hepatocellular nuclei. Both LMW-HA-induced TNF-alpha production and NF-kappaB translocation were blocked by pretreatment with PDTC. Our findings provide evidence for an unknown mechanism of LMW-HA-dependent protection from inflammatory liver disease, i.e., induction of TNF-alpha- and NF-kappaB-dependent cytoprotective proteins within the target parenchymal liver cells.

AB - Liver resident NK1.1+ T cells are supposed to play a pivotal role in the onset of inflammatory liver injury in experimental mouse models such as concanavalin A (Con A)-induced hepatitis. These cells, expressing the adhesion receptor, CD44, are largely depleted from the liver by a single intravenous injection of low-molecular-weight fragments of hyaluronic acid (LMW-HA). Here, we report that LMW-HA pretreatment protected mice from liver injury in several models of T-cell- and macrophage-dependent, tumor necrosis factor alpha (TNF-alpha)-mediated inflammatory liver injury, i.e., from liver injury induced by either Con A or Pseudomonas exotoxin A (PEA) or PEA/lipopolysaccharide (LPS). Interestingly, apart from inhibition of cellular adhesion, pretreatment of mice with LMW-HA was also capable of preventing hepatocellular apoptosis and activation of caspase-3 induced by direct administration of recombinant murine (rmu) TNF-alpha to D-galactosamine (GalN)-sensitized mice. LMW-HA-induced hepatoprotection could be neutralized by pretreatment with the nuclear factor-kappaB (NF-kappaB) inhibitor, pyrrolidine dithiocarbamate (PDTC), demonstrating the involvement of NF-kappaB in the observed protective mechanism. Indeed, injection of LMW-HA rapidly induced the production of TNF-alpha by Kupffer cells and the translocation of NF-kappaB into hepatocellular nuclei. Both LMW-HA-induced TNF-alpha production and NF-kappaB translocation were blocked by pretreatment with PDTC. Our findings provide evidence for an unknown mechanism of LMW-HA-dependent protection from inflammatory liver disease, i.e., induction of TNF-alpha- and NF-kappaB-dependent cytoprotective proteins within the target parenchymal liver cells.

KW - Animals

KW - Male

KW - Mice

KW - Mice, Inbred BALB C

KW - CD4 Lymphocyte Count

KW - Molecular Weight

KW - Lymphocyte Count

KW - Concanavalin A/pharmacology

KW - Lipopolysaccharides/pharmacology

KW - ADP Ribose Transferases

KW - Antigens, CD44/analysis

KW - Bacterial Toxins

KW - Cell Death/drug effects

KW - Cytokines/blood

KW - Drug-Induced Liver Injury/pathology/prevention & control

KW - Exotoxins/pharmacology

KW - Hyaluronic Acid/chemistry/pharmacology

KW - Kupffer Cells/metabolism

KW - Liver/pathology

KW - Liver Failure/etiology/prevention & control

KW - Macrophages/physiology

KW - NF-kappa B/antagonists & inhibitors/physiology

KW - T-Lymphocytes/immunology/pathology/physiology

KW - Tumor Necrosis Factor-alpha

KW - Virulence Factors