Inhibition of the multiplication ofListeria monocytogenesin a murine hepatocyte cell line (ATCC TIB73) by IFN-γ and TNF-α

1996 ◽  
Vol 20 (5) ◽  
pp. 287-295 ◽  
Author(s):  
Ronnarit Haponsaph ◽  
Charles J. Czuprynski
Keyword(s):  
Cell Line ◽  
Hepatocyte Cell Line ◽  
Tnf Α ◽  
Ifn Γ ◽  
Murine Hepatocyte

Enhancement of survival by LPA via Erk1/Erk2 and PI 3-kinase/Akt pathways in a murine hepatocyte cell line

2001 ◽  
Vol 281 (6) ◽  
pp. C2010-C2019 ◽  
Author(s):  
Yuri Y. Sautin ◽  
James M. Crawford ◽  
Stanislav I. Svetlov
Keyword(s):  
Cell Line ◽  
Mitogen Activated Protein Kinase ◽  
Dependent Manner ◽  
Protective Effects ◽  
Hepatocellular Injury ◽  
Cell Protection ◽  
Lpa Receptor ◽  
Hepatocyte Cell Line ◽  
Tnf Α ◽  
Murine Hepatocyte

First published September 5, 2001; 10.1152/ajpcell.00077.2001.—Protective mechanisms for lysophosphatidic acid (LPA) against cell death caused by Clostridium difficile toxin, or tumor necrosis factor-α (TNF-α) plus d-galactosamine, were investigated in a murine hepatocyte cell line AML12 expressing Edg2 LPA receptor. In these models of hepatocellular injury, LPA prevented hepatocyte damage, suppressed apoptosis, and enhanced cell survival in a dose-dependent fashion. The protective effects of LPA were abolished by wortmannin and LY-294002, specific inhibitors of phosphatidylinositol 3-phosphate kinase (PI 3-kinase), and by PD-98059 and U-0126, inhibitors of MEK1/MEK2. In nontreated hepatocytes, LPA elicited a gradual and sustained increase in phosphorylation of Erk1/Erk2 over 180 min of stimulation and downstream phosphorylation of p90RSK and transcription factor Elk-1. In C. difficile toxin-treated cells, LPA-induced phosphorylation of Erk1/Erk2 was rapid but transient, while p90RSK and Elk-1 phosphorylation did not change significantly. LPA stimulated phosphorylation of Akt in a time-dependent manner in both intact and toxin-treated AML12 hepatocytes. Wortmannin and LY-294002 abolished phosphorylation of Akt, further supporting activation of PI 3-kinase/Akt as a signaling pathway, which mediates hepatocyte protection by LPA. Taken together, these results demonstrate that LPA prevents cell apoptosis induced by C. difficile toxin and TNF-α/d-galactosamine in the AML12 murine hepatocyte cell line. Cell protection by LPA involves activation of the mitogen-activated protein kinase Erk1/Erk2 cascade and PI 3-kinase-dependent phosphorylation of Akt.

scholarly journals Ivermectin induces P-glycoprotein expression and function through mRNA stabilization in murine hepatocyte cell line

2012 ◽  
Vol 83 (2) ◽  
pp. 269-278 ◽  
Author(s):  
Cécile Ménez ◽  
Laïla Mselli-Lakhal ◽  
Magali Foucaud-Vignault ◽  
Patrick Balaguer ◽  
Michel Alvinerie ◽  
...  
Keyword(s):  
Cell Line ◽  
Mrna Stabilization ◽  
Hepatocyte Cell Line ◽  
P Glycoprotein ◽  
And Function ◽  
Murine Hepatocyte

scholarly journals Lambda Interferon Inhibits Hepatitis B and C Virus Replication

2005 ◽  
Vol 79 (6) ◽  
pp. 3851-3854 ◽  
Author(s):  
Michael D. Robek ◽  
Bryan S. Boyd ◽  
Francis V. Chisari
Keyword(s):  
Hepatitis B ◽  
Receptor Complex ◽  
Hbv Replication ◽  
Hepatocyte Cell Line ◽  
Huh7 Cells ◽  
B Virus ◽  
Ifn Γ ◽  
Chronic Hbv ◽  
Β Receptor ◽  
Murine Hepatocyte

ABSTRACT Lambda interferon (IFN-λ) induces an intracellular IFN-α/β-like antiviral response through a receptor complex distinct from the IFN-α/β receptor. We therefore determined the ability of IFN-λ to inhibit hepatitis B virus (HBV) and hepatitis C virus (HCV) replication. IFN-λ inhibits HBV replication in a differentiated murine hepatocyte cell line with kinetics and efficiency similar to IFN-α/β and does not require the expression of IFN-α/β or IFN-γ. Furthermore, IFN-λ blocked the replication of a subgenomic and a full-length genomic HCV replicon in human hepatocyte Huh7 cells. These results suggest the possibility that IFN-λ may be therapeutically useful in the treatment of chronic HBV or HCV infection.

Zinc modulates mRNA levels of cytokines

2003 ◽  
Vol 285 (5) ◽  
pp. E1095-E1102 ◽  
Author(s):  
Bin Bao ◽  
Ananda S. Prasad ◽  
Frances W. J. Beck ◽  
Michele Godmere
Keyword(s):  
Gene Expression ◽  
Cell Line ◽  
Zinc Deficiency ◽  
Mrna Levels ◽  
Macrophage Cell Line ◽  
Macrophage Cell ◽  
Th1 Cell ◽  
Killer Activity ◽  
Tnf Α ◽  
Ifn Γ

Zinc plays an important role in cell-mediated immune function. Altered cellular immune response resulting from zinc deficiency leads to frequent microbial infections, thymic atrophy, decreased natural killer activity, decreased thymic hormone activity, and altered cytokine production. In this study, we examined the effect of zinc deficiency on IL-2 and IFN-γ in HUT-78 (Th0) and D1.1 (Th1) cell lines and TNF-α, IL-1β, and IL-8 in the HL-60 (monocyte-macrophage) cell line. The results demonstrate that zinc deficiency decreased the levels of IL-2 and IFN-γ cytokines and mRNAs in HUT-78 after 6 h of PMA/ p-phytohemagglutinin (PHA) stimulation and in D1.1 cells after 6 h of PHA/ionomycin stimulation compared with the zinc-sufficient cells. However, zinc deficiency increased the levels of TNF-α, IL-1β, and IL-8 cytokines and mRNAs in HL-60 cells after 6 h of PMA stimulation compared with zinc-sufficient cells. Actinomycin D study suggests that the changes in the levels of these cytokine mRNAs were not the result of the stability affected by zinc but might be the result of altered expression of these cytokine genes. These data demonstrate that zinc mediates positively the gene expression of IL-2 and IFN-γ in the Th1 cell line and negatively TNF-α, IL-1β, and IL-8 in the monocyte-macrophage cell line. Our study shows that the effect of zinc on gene expression and production of cytokines is cell lineage specific.

Silica-induced chemokine expression in alveolar type II cells is mediated by TNF-α

1998 ◽  
Vol 275 (6) ◽  
pp. L1110-L1119 ◽  
Author(s):  
Edward G. Barrett ◽  
Carl Johnston ◽  
Günter Oberdörster ◽  
Jacob N. Finkelstein
Keyword(s):  
Epithelial Cells ◽  
Cell Line ◽  
Rnase Protection Assay ◽  
Alveolar Type ◽  
Mrna Levels ◽  
Type Ii ◽  
Rnase Protection ◽  
Tnf Α ◽  
Type Ii Cell ◽  
Ifn Γ

Recent evidence has suggested that epithelial cells may contribute to the inflammatory response in the lung after exposure to crystalline silica through the production of and response to specific growth factors, chemokines, and cytokines. However, the exact cellular and molecular responses of epithelial cells to silica exposure remains unclear. Using a murine alveolar type II cell line [murine lung epithelial (MLE)-15 cell line], we measured the early changes in various cytokine and chemokine mRNA species after exposure of the cells to 4–35 μg/cm2 of silica (cristobalite), interferon (IFN)-γ, tumor necrosis factor (TNF)-α, and lipopolysaccharide (LPS) alone or in combination. Total mRNA was isolated and assayed with an RNase protection assay after 6 and 24 h of exposure. Cristobalite exposure alone led to an increase in monocyte chemotactic protein (MCP)-1, macrophage inflammatory protein (MIP)-2, and regulated on activation normal T cells expressed and secreted (RANTES) mRNAs. Treatment with IFN-γ alone increased MCP-1 mRNA levels. Treatment with TNF-α or LPS alone led to an increase in MCP-1 and MIP-2 mRNA. The combination of cristobalite plus TNF-α led to an additive increase in MCP-1 and MIP-2, whereas cristobalite plus IFN-γ or LPS had a synergistic effect. We also found with a TNF-α-neutralizing antibody that TNF-α plays a major role in mediating the type II cell chemokine response to cristobalite exposure. The results indicate that the cristobalite-induced chemokine response in the lung epithelium is mediated in part by TNF-α and can be enhanced by macrophage- and lymphocyte-derived inflammatory mediators in an additive and synergistic fashion.

scholarly journals Introduction of a murine p53 mutation corresponding to human codon 249 into a murine hepatocyte cell line results in growth advantage, but not in transformation

Hepatology ◽  
1995 ◽  
Vol 22 (4) ◽  
pp. 1279-1288 ◽  
Author(s):  
Luba Dumenco ◽  
Delphine Oguey ◽  
Justina Wu ◽  
Norma Messier ◽  
Nelson Fausto
Keyword(s):  
Cell Line ◽  
P53 Mutation ◽  
Hepatocyte Cell Line ◽  
Murine Hepatocyte

Thyroid hormone responsive genes in the murine hepatocyte cell line AML 12

Gene ◽  
2007 ◽  
Vol 396 (2) ◽  
pp. 332-337 ◽  
Author(s):  
Tereza Ventura-Holman ◽  
Abulkhair Mamoon ◽  
Joseph F. Maher ◽  
Jose S. Subauste
Keyword(s):  
Thyroid Hormone ◽  
Cell Line ◽  
Hepatocyte Cell Line ◽  
Murine Hepatocyte

scholarly journals Immune-Regulatory and Molecular Effects of Antidepressants on the Inflamed Human Keratinocyte HaCaT Cell Line

2021 ◽  
Author(s):  
Curzytek K. ◽  
Maes M. ◽  
Kubera M.
Keyword(s):  
Cell Line ◽  
Inflammatory Cytokines ◽  
Molecular Mechanisms ◽  
Hacat Cell ◽  
Antidepressant Drugs ◽  
Skin Inflammation ◽  
Hacat Cell Line ◽  
Tnf Α ◽  
Ifn Γ ◽  
Pro Inflammatory Cytokines

AbstractAllergic contact dermatitis (ACD) is a T cell-mediated type of skin inflammation resulting from contact hypersensitivity (CHS) to antigens. There is strong comorbidity between ACD and major depression. Keratinocytes release immunomodulatory mediators including pro-inflammatory cytokines and chemokines, which modulate skin inflammation and are crucial cell type for the development of CHS. Our previous studies showed that fluoxetine and desipramine were effective in suppressing CHS in different mouse strains. However, the immune and molecular mechanisms underlying this effect remain to be explored. The aim of the current study was to determine the immune and molecular mechanisms of action of antidepressant drugs engaged in the inhibition of CHS response in the stimulated keratinocyte HaCaT cell line. The results show that LPS, TNF-α/IFN-γ, and DNFB stimulate HaCaT cells to produce large amounts of pro-inflammatory factors including IL-1β, IL-6, CCL2, and CXCL8. HaCaT stimulation was associated with increased expression of ICAM-1, a cell adhesion molecule, and decreased expression of E-cadherin. Imipramine, desipramine, and fluoxetine suppress the production of IL-1β, CCL2, as well as the expression of ICAM-1. LPS and TNF-α/IFN-γ activate p-38 kinase, but antidepressants do not regulate this pathway. LPS decreases E-cadherin protein expression and fluoxetine normalizes these effects. In summary, the antidepressant drugs examined in this study attenuate the stimulated secretion of pro-inflammatory cytokines, chemokines, and modulate adhesion molecule expression by the HaCaT cell line. Therefore, antidepressants may have some clinical efficacy in patients with ACD and patients with comorbid depression and contact allergy.

scholarly journals Human Wharton’s Jelly Stem Cell Secretions Inhibit Human Leukemic Cell Line K562 in vitro by Inducing Cell Cycle Arrest and Apoptosis

2021 ◽  
Vol 9 ◽  
Author(s):  
Muneerah A. H. Huwaikem ◽  
Gauthaman Kalamegam ◽  
Ghadeer Alrefaei ◽  
Farid Ahmed ◽  
Roaa Kadam ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Stem Cell ◽  
Cell Cycle Arrest ◽  
Cell Line ◽  
Inflammatory Cytokine ◽  
K562 Cells ◽  
Cycle Arrest ◽  
Tnf Α ◽  
Ifn Γ

Emerging resistance to the tyrosine kinase inhibitors that target the BCR-ABL1 oncoprotein has prompted research for novel therapeutics against chronic myeloid leukemia (CML). Herein, we evaluated the tumor inhibitory properties of the human Wharton’s jelly stem cells (hWJSCs) co-culture (hWJSC-CC) and their extracts, namely, the hWJSC-conditioned medium (hWJSC-CM; 100%) and hWJSC-lysate (hWJSC-L; 15 μg/ml), on a CML cell line K562 in vitro. The hWJSCs expressed mesenchymal stem cell (MSC)-related cluster of differentiation (CD) markers and demonstrated mesodermal tissue differentiation potential. The cell metabolic activity showed a mean maximal decrease in the K562 cells by 49.12, 41.98, and 68.80% following treatment with the hWJSC-CC, hWJSC-CM, and hWJSC-L, respectively, at 72 h. The sub-G1 population in the cell cycle was decreased by 3.2, 4.5, and 3.8% following treatment with the hWJSC-CC, hWJSC-CM, and hWJSC-L, whereas the G2/M cell population was increased by 13.7 and 12.5% with the hWJSC-CM and hWJSC-L, respectively, at 48 h. Annexin V–allophycocyanin (APC) assay showed an increase in the apoptotic cells by 4.0, 3.9, and 4.5% at 48 h. The expression of pro-apoptotic BAX and CASP3 genes were increased, whereas BIRC5 (Survivin) was decreased compared with the control. The pro-inflammation-related genes, namely, IFN-γ, TNF-α, IL-1β, IL-6, IL-8, and IL-12A, were decreased, whereas the anti-inflammatory genes, namely, IL-4 and IL-10, were increased following treatment with the hWJSC-CC, hWJSC-CM, and hWJSC-L at 48 h. Multiplex bead-based cytokine assay also demonstrated decreases in the pro-inflammatory cytokines (IFN-γ, TNF-α, IL-1β, IL-6, and IL-12) and an increase in the anti-inflammatory cytokine (IL-10) compared with the control. The pro-inflammatory cytokine IL-8 showed an increase with the hWJSC-CC and decreases with both the hWJSC-CM and the hWJSC-L. The hWJSCs and their extracts inhibited the K562 cells by causing cell cycle arrest and inducing apoptosis via the soluble cellular factors. However, an in vivo evaluation is necessary to unravel the true potential of the hWJSCs and their extracts before its use in CML inhibition.

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