5 results on '"Arshad, Muhammad Imran"'
Search Results
2. Oncostatin M induces IL-33 expression in liver endothelial cells in mice and expands ST2+CD4+lymphocytes
- Author
-
Arshad, Muhammad Imran, primary, Guihard, Pierre, additional, Danger, Yannic, additional, Noel, Gregory, additional, Le Seyec, Jacques, additional, Boutet, Marie-Astrid, additional, Richards, Carl D., additional, L'Helgoualc'h, Annie, additional, Genet, Valentine, additional, Lucas-Clerc, Catherine, additional, Gascan, Hugues, additional, Blanchard, Frédéric, additional, Piquet-Pellorce, Claire, additional, and Samson, Michel, additional
- Published
- 2015
- Full Text
- View/download PDF
3. Oncostatin M induces IL-33 expression in liver endothelial cells in mice and expands ST2+CD4+ lymphocytes.
- Author
-
Arshad, Muhammad Imran, Guihard, Pierre, Danger, Yannic, Noel, Gregory, Le Seyec, Jacques, Boutet, Marie-Astrid, Richards, Carl D., L'Helgoualc'h, Annie, Genet, Valentine, Lucas-Clerc, Catherine, Gascan, Hugues, Blanchard, Frédéric, Piquet-Pellorce, Claire, and Samson, Michel
- Subjects
- *
ONCOSTATIN M , *INTERLEUKIN-33 , *GENE expression , *LIVER cells , *INTRAMUSCULAR injections , *LABORATORY mice - Abstract
Interleukin (IL)-33 is crucially involved in liver pathology and drives hepatoprotective functions. However, the regulation of IL-33 by cytokines of the IL-6 family, including oncostatin M (OSM) and IL-6, is not well studied. The aim of the present study was to determine whether OSM mediates regulation of IL-33 expression in liver cells. Intramuscular administration in mice of an adenovirus encoding OSM (AdOSM) leads to increase in expression of OSM in muscles, liver, and serum of AdOSM-infected mice compared with control mice. The increase of circulating OSM markedly regulated mRNA of genes associated with blood vessel biology, chemotaxis, cellular death, induction of cell adhesion molecules, and the alarmin cytokine IL-33 in liver. Steady-state IL-33 mRNA was upregulated by OSM at an early phase (8 h) following AdOSM infection. At the protein level, the expression of IL-33 was significantly induced in liver endothelial cells [liver sinusoidal endothelial cells (LSEC) and vascular endothelial cells] with a peak at 8 days post-AdOSM infection in mice. In addition, we found OSM-stimulated human microvascular endothelial HMEC-1 cells and human LSEC/TRP3 cells showed a significant increase in expression of IL-33 mRNA in a dose-dependent manner in cell culture. The OSM-mediated overexpression of IL-33 was associated with the activation/enrichment of CD4+ST2+ cells in liver of AdOSM-infected mice compared with adenovirus encoding green fluorescent protein-treated control mice. In summary, these data suggest that the cytokine OSM regulates the IL-33 expression in liver endothelial cells in vivo and in HMEC-1/TRP3 cells in vitro and may specifically expand the target CD4+ST2+ cells in liver. [ABSTRACT FROM AUTHOR]
- Published
- 2015
- Full Text
- View/download PDF
4. Ablation of interaction between IL-33 and ST2+ regulatory T cells increases immune cell-mediated hepatitis and activated NK cell liver infiltration.
- Author
-
Noel G, Arshad MI, Filliol A, Genet V, Rauch M, Lucas-Clerc C, Lehuen A, Girard JP, Piquet-Pellorce C, and Samson M
- Subjects
- Animals, Cells, Cultured, Chemical and Drug Induced Liver Injury metabolism, Chemical and Drug Induced Liver Injury pathology, Chemical and Drug Induced Liver Injury prevention & control, Chemotaxis, Leukocyte, Concanavalin A, Cytokines immunology, Cytokines metabolism, Disease Models, Animal, Genetic Predisposition to Disease, Hepatitis metabolism, Hepatitis pathology, Hepatitis prevention & control, Inflammation Mediators immunology, Inflammation Mediators metabolism, Interleukin-1 Receptor-Like 1 Protein metabolism, Interleukin-33 genetics, Killer Cells, Natural metabolism, Liver metabolism, Mice, Inbred C57BL, Mice, Knockout, Phenotype, Signal Transduction, T-Lymphocytes, Regulatory metabolism, Chemical and Drug Induced Liver Injury immunology, Hepatitis immunology, Interleukin-1 Receptor-Like 1 Protein immunology, Interleukin-33 deficiency, Killer Cells, Natural immunology, Liver innervation, Lymphocyte Activation, T-Lymphocytes, Regulatory immunology
- Abstract
The IL-33/ST2 axis plays a protective role in T-cell-mediated hepatitis, but little is known about the functional impact of endogenous IL-33 on liver immunopathology. We used IL-33-deficient mice to investigate the functional effect of endogenous IL-33 in concanavalin A (Con A)-hepatitis. IL-33(-/-) mice displayed more severe Con A liver injury than wild-type (WT) mice, consistent with a hepatoprotective effect of IL-33. The more severe hepatic injury in IL-33(-/-) mice was associated with significantly higher levels of TNF-α and IL-1β and a larger number of NK cells infiltrating the liver. The expression of Th2 cytokines (IL-4, IL-10) and IL-17 was not significantly varied between WT and IL-33(-/-) mice following Con A-hepatitis. The percentage of CD25(+) NK cells was significantly higher in the livers of IL-33(-/-) mice than in WT mice in association with upregulated expression of CXCR3 in the liver. Regulatory T cells (Treg cells) strongly infiltrated the liver in both WT and IL-33(-/-) mice, but Con A treatment increased their membrane expression of ST2 and CD25 only in WT mice. In vitro, IL-33 had a significant survival effect, increasing the total number of splenocytes, including B cells, CD4(+) and CD8(+) T cells, and the frequency of ST2(+) Treg cells. In conclusion, IL-33 acts as a potent immune modulator protecting the liver through activation of ST2(+) Treg cells and control of NK cells., (Copyright © 2016 the American Physiological Society.)
- Published
- 2016
- Full Text
- View/download PDF
5. Oncostatin M induces IL-33 expression in liver endothelial cells in mice and expands ST2+CD4+ lymphocytes.
- Author
-
Arshad MI, Guihard P, Danger Y, Noel G, Le Seyec J, Boutet MA, Richards CD, L'Helgoualc'h A, Genet V, Lucas-Clerc C, Gascan H, Blanchard F, Piquet-Pellorce C, and Samson M
- Subjects
- Animals, Cell Culture Techniques, Endothelial Cells drug effects, Endothelium, Vascular drug effects, Endothelium, Vascular metabolism, Flow Cytometry, Hepatocytes drug effects, Humans, Interleukin-33 genetics, Liver metabolism, Male, Mice, Mice, Inbred C57BL, RNA, Messenger genetics, Reverse Transcriptase Polymerase Chain Reaction, CD4-Positive T-Lymphocytes drug effects, Endothelial Cells metabolism, Growth Inhibitors pharmacology, Interleukin-33 metabolism, Liver drug effects, Oncostatin M pharmacology
- Abstract
Interleukin (IL)-33 is crucially involved in liver pathology and drives hepatoprotective functions. However, the regulation of IL-33 by cytokines of the IL-6 family, including oncostatin M (OSM) and IL-6, is not well studied. The aim of the present study was to determine whether OSM mediates regulation of IL-33 expression in liver cells. Intramuscular administration in mice of an adenovirus encoding OSM (AdOSM) leads to increase in expression of OSM in muscles, liver, and serum of AdOSM-infected mice compared with control mice. The increase of circulating OSM markedly regulated mRNA of genes associated with blood vessel biology, chemotaxis, cellular death, induction of cell adhesion molecules, and the alarmin cytokine IL-33 in liver. Steady-state IL-33 mRNA was upregulated by OSM at an early phase (8 h) following AdOSM infection. At the protein level, the expression of IL-33 was significantly induced in liver endothelial cells [liver sinusoidal endothelial cells (LSEC) and vascular endothelial cells] with a peak at 8 days post-AdOSM infection in mice. In addition, we found OSM-stimulated human microvascular endothelial HMEC-1 cells and human LSEC/TRP3 cells showed a significant increase in expression of IL-33 mRNA in a dose-dependent manner in cell culture. The OSM-mediated overexpression of IL-33 was associated with the activation/enrichment of CD4(+)ST2(+) cells in liver of AdOSM-infected mice compared with adenovirus encoding green fluorescent protein-treated control mice. In summary, these data suggest that the cytokine OSM regulates the IL-33 expression in liver endothelial cells in vivo and in HMEC-1/TRP3 cells in vitro and may specifically expand the target CD4(+)ST2(+) cells in liver., (Copyright © 2015 the American Physiological Society.)
- Published
- 2015
- Full Text
- View/download PDF
Catalog
Discovery Service for Jio Institute Digital Library
For full access to our library's resources, please sign in.