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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Bae, Ki Beom Ryoo, Zae Young Kim, Hei Jung Ji, Young Rae Kim, Myoung Ok Lee, Sanggyu |
| Description | Author Affiliation: Ji YR ( From the School of Life Science, KNU Creative BioResearch Group (BK21 Plus Project), Kyungpook National University, Buk-gu, Daegu 702-701, Korea and.); Kim HJ ( From the School of Life Science, KNU Creative BioResearch Group (BK21 Plus Project), Kyungpook National University, Buk-gu, Daegu 702-701, Korea and.); Bae KB ( From the School of Life Science, KNU Creative BioResearch Group (BK21 Plus Project), Kyungpook National University, Buk-gu, Daegu 702-701, Korea and.); Lee S ( From the School of Life Science, KNU Creative BioResearch Group (BK21 Plus Project), Kyungpook National University, Buk-gu, Daegu 702-701, Korea and.); Kim MO ( the Department of Animal Science, Kyungpook National University, Sangju 742-711, Korea.); Ryoo ZY ( From the School of Life Science, KNU Creative BioResearch Group (BK21 Plus Project), Kyungpook National University, Buk-gu, Daegu 702-701, Korea and jaewoong64@hanmail.net.) |
| Abstract | Serum amyloid A is a proinflammatory molecule that induces leukocyte infiltration and promotes neutrophil adhesion to endothelial cells under inflammatory conditions. The aim of this study was to examine whether Saa1 aggravates T cell-mediated hepatitis by inducing chemokines in a liver-specific, Saa1-overexpressing, transgenic (TG) mouse model. We generated TG mice in which Saa1 was overexpressed specifically in liver tissue. The chemokines monocyte chemotactic protein 1 (MCP1), MIP1 , MIP1ß, interferon γ-induced protein 10 (IP-10), and eotaxin were induced in Saa1 TG mice. After concanavalin A treatment, Saa1 expression was higher in Saa1 TG mice than in WT mice. More severe liver injury, increased hepatocyte apoptosis, and higher levels of hepatic enzymes were observed in Saa1 TG mice than in WT mice. Liver infiltration of CD4(+) T cells and macrophages increased after inducing hepatitis. Activation of T cells was higher in Saa1 TG mice than in WT mice, and the populations of Th17 cells and regulatory T cells were altered by overexpressing Saa1 in TG mice. Secretion of various cytokines, such as interferon γ, tumor necrosis factor , and interleukin 6, increased in Saa1 TG mice. Injecting a Toll-like receptor 2 (TLR2) antagonist in vivo inhibited chemokine expression and IκB phosphorylation and showed that the induction of chemokines by Saa1 was dependent on TLR2. Hepatic Saa1 accelerated T cell-mediated hepatitis by inducing chemokine production and activating T cells by TLR2. Therefore, Saa1 might be a novel inflammatory factor that acts as a chemokine modulator in hepatitis. |
| ISSN | 00219258 |
| e-ISSN | 1083351X |
| Journal | Journal of Biological Chemistry |
| Issue Number | 20 |
| Volume Number | 290 |
| Language | English |
| Publisher | American Society for Biochemistry and Molecular Biology (United States) |
| Publisher Date | 2015-05-15 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Drug-Induced Liver Injury Metabolism Chemokines Biosynthesis Inflammation Mediators Serum Amyloid A Protein T-Lymphocytes, Regulatory Th17 Cells Toll-Like Receptor 2 Animals Genetics Pathology Concanavalin A Adverse Effects Pharmacology Liver Lymphocyte Activation Drug Effects Macrophages Mice Mice, Transgenic Mitogens Antagonists & Inhibitors Research Support, Non-U.S. Gov't Biochemistry Molecular Biology |
| Content Type | Text |
| Resource Type | Article |
| Subject | Cell Biology Biochemistry Molecular Biology |
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