ArticleThe Journal of biological chemistry2015
Hepatic serum amyloid A1 aggravates T cell-mediated hepatitis by inducing chemokines via Toll-like receptor 2 in mice.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 43 citations in OpenAlex.
- Systemically delivered lipid nanoparticle-mRNA encoding lysosomal acid β-glucosidase restores the enzyme deficiency in a murine Gaucher disease model.Gene therapy · 2025Article
- Diagnostics of Autoimmune Hepatitis Enabled by Non-Invasive Clinical Proteomics.Alimentary pharmacology & therapeutics · 2025Observational
- Inflammation and immunity in liver homeostasis and disease: a nexus of hepatocytes, nonparenchymal cells and immune cells.Cellular & molecular immunology · 2025Review
- Recent Advances in Studies of Serum Amyloid A: Implications in Inflammation, Immunity and Tumor Metastasis.International journal of molecular sciences · 2025Review
- Co-occurrence of autoimmune diseases and metabolic disorders in familial mediterranean fever patients: review of literature and case reports.Frontiers in immunology · 2025Review
- Shared inflammatory glial cell signature after stab wound injury, revealed by spatial, temporal, and cell-type-specific profiling of the murine cerebral cortex.Nature communications · 2024Article
- Serum amyloid A and metabolic disease: evidence for a critical role in chronic inflammatory conditions.Frontiers in cardiovascular medicine · 2023Review
- Hepatitis C Core Protein Induces a Genotype-Specific Susceptibility of Hepatocytes to TNF-Induced Death In Vitro and In Vivo.Viruses · 2022Article
- Characterization of Hepatic Dysfunction in Subjects Diagnosed With Chronic GVHD by NIH Consensus Criteria.Transplantation and cellular therapy · 2022Article
- Effects of serum amyloid protein A on influenza A virus replication and viral interactions with neutrophils.Journal of leukocyte biology · 2021Article
- Toll-like receptor 2 activation and up-regulation by high mobility group box-1 contribute to post-operative neuroinflammation and cognitive dysfunction in mice.Journal of neurochemistry · 2021Article
- Review
- SAA1/TLR2 axis directs chemotactic migration of hepatic stellate cells responding to injury.iScience · 2021Article
- Plasma proteomic analysis of autoimmune hepatitis in an improved AIH mouse model.Journal of translational medicine · 2020Article
- Serum Amyloid A1 (SAA1) Revisited: Restricted Leukocyte-Activating Properties of Homogeneous SAA1.Frontiers in immunology · 2020Article
- Serum amyloid A1 is involved in amyloid plaque aggregation and memory decline in amyloid beta abundant condition.Transgenic research · 2019Article
- The JAK inhibitor tofacitinib ameliorates immune‑mediated liver injury in mice.Molecular medicine reports · 2019Article
- Serum amyloid A - a review.Molecular medicine (Cambridge, Mass.) · 2018Review
- Serum amyloid A primes microglia for ATP-dependent interleukin-1β release.Journal of neuroinflammation · 2018Article
- Amantadine attenuates sepsis-induced cognitive dysfunction possibly not through inhibiting toll-like receptor 2.Journal of molecular medicine (Berlin, Germany) · 2018Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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), MIP1α, MIP1β, 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 α, and interleukin 6, increased in Saa1 TG mice. Injecting a Toll-like receptor 2 (TLR2) antagonist in vivo inhibited chemokine expression and IκBα 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.
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