ArticleClinical and experimental immunology1992
Production of serum amyloid A and C-reactive protein by HepG2 cells stimulated with combinations of cytokines or monocyte conditioned media: the effects of prednisolone.
Article in Clinical and experimental immunology, 1992. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 62 citations in OpenAlex.
- The multi-biomarker disease activity test for assessing response to treatment strategies using methotrexate with or without prednisone in the CAMERA-II trial.Arthritis research & therapy · 2020Trial
- The acute phase protein response in patients receiving subcutaneous IL-6.Clinical and experimental immunology · 1995Trial
- From IL-6 production to IL-6R buffering: a unified IL-6-IL-6R framework for immune homeostasis during viral infection.Frontiers in immunology · 2026Review
- Review
- Combined repetitive transcranial magnetic stimulation and medication treatment for depression is associated with serum amyloid a level: Evidence from naturalistic clinical practice.Frontiers in neuroscience · 2022Article
- Inflammation Induces Changes in the Functional Expression of P-gp, BCRP, and MRP2: An Overview of Different Models and Consequences for Drug Disposition.Pharmaceutics · 2021Review
- Article
- Serum Amyloid A1 Is an Epithelial Prorestitutive Factor.The American journal of pathology · 2018Article
- The cytokine-serum amyloid A-chemokine network.Cytokine & growth factor reviews · 2016Review
- Review
- Differential influence of p38 mitogen activated protein kinase (MAPK) inhibition on acute phase protein synthesis in human hepatoma cell lines.Annals of the rheumatic diseases · 2006Article
- Macrophage conditioned medium induces the expression of C-reactive protein in human aortic endothelial cells: potential for paracrine/autocrine effects.The American journal of pathology · 2005Article
- Impaired degradation of serum amyloid A (SAA) protein by cytokine-stimulated monocytes.Clinical and experimental immunology · 2001Article
- Interleukin-6 is necessary, but not sufficient, for induction of the humanC-reactive protein gene in vivo.The Biochemical journal · 1997Article
- Serum amyloid A protein enhances the activity of secretory non-pancreatic phospholipase A2.The Biochemical journal · 1995Article
- IL-1 receptor antagonist (IL-1Ra) does not inhibit the production of C-reactive protein or serum amyloid A protein by human primary hepatocytes. Differential regulation in normal and tumour cells.Clinical and experimental immunology · 1995Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The hepatic production of the acute phase proteins in response to inflammatory cytokines, and the interaction of corticosteroids within this response, has been the subject of considerable recent research. In this study we have examined the effects of the corticosteroid prednisolone on the production of IL-1 alpha and IL-1 beta by lipopolysaccharide (LPS)-stimulated monocytes, and the ability of the monocyte conditioned media (MOCM) obtained under these conditions to induce human hepatoma HepG2 cells to produce serum amyloid A (SAA) and C-reactive protein (CRP). We also examined the production of SAA and CRP by HepG2 cells exposed to different combinations and concentrations of recombinant human (rh) IL-1 alpha, rhIL-1 beta, rhIL-6, recombinant human tumour necrosis factor-alpha (rhTNF-alpha) and prednisolone. The findings indicate: (i) prednisolone substantially inhibits the production of both IL-1 alpha and IL-1 beta by LPS-stimulated monocytes. The MOCM from prednisolone-treated monocytes induced less SAA and CRP production by HepG2 cells; (ii) IL-1 alpha and IL-1 beta both induced CRP and SAA synthesis by HepG2 cells, but only in the presence of IL-6. IL-1 beta was the more potent inducer for SAA production, but for CRP production IL-1 alpha and IL-1 beta were equivalent; (iii) prednisolone enhances the production of SAA by HepG2 cells, but does not enhance the production of CRP; (iv) TNF-alpha in the presence or absence of IL-6 and/or prednisolone did not induce the production of SAA or CRP by HepG2 cells. These findings offer a tenable solution to a disparate production of SAA compared with CRP in corticosteroid-treated cystic fibrosis (CF) patients.
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