Abstract | AIM: METHODS: Cultured human OF were incubated with recombinant interleukin 1 beta (rIL-1 beta; 0.2, 2.0, 20 ng/ml) alone or incubated with rIL-1 beta and DEX (10(-8), 10(-7), 10(-6) M) or CSA (3, 30, 300 ng/ml) for 24 hours. ELISA and northern blot analyses were performed to determine OF IL-8 and MCP-1 protein secretion and mRNA expression, respectively. RESULTS: OF lacked constitutive IL-8 or MCP-1 expression, but secreted significant amounts of these chemokines and expressed substantial steady state mRNA for both chemokines upon rIL-1 beta stimulation. DEX caused dose dependent inhibition of IL-1 induced IL-8 (p < 0.001) and MCP-1 (p < 0.05) secretion and mRNA expression at all concentrations of rIL-1 beta. CSA enhanced IL-1 induced OF IL-8 (p < 0.001) and suppressed rIL-1 beta induced OF MCP-1 (p < 0.05) secretion when lower doses of rIL-1 beta were used. These effects on secreted chemokines at different concentrations of rIL-1 beta and immunomodulating agents were corroborated by steady state OF IL-8 and MCP-1 mRNA expression. CONCLUSIONS: DEX is a potent inhibitor of OF IL-8 and MCP-1. In contrast, CSA enhances IL-1 induced OF IL-8 and suppresses OF MCP-1. These observations may explain the relative lack of CSA effectiveness in human orbital diseases that respond to corticosteroids.
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Authors | M A Burnstine, S G Elner, V M Elner |
Journal | The British journal of ophthalmology
(Br J Ophthalmol)
Vol. 82
Issue 3
Pg. 318-22
(Mar 1998)
ISSN: 0007-1161 [Print] England |
PMID | 9602633
(Publication Type: Journal Article, Research Support, U.S. Gov't, P.H.S.)
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Chemical References |
- Anti-Inflammatory Agents
- Chemokine CCL2
- Chemokines
- Immunosuppressive Agents
- Interleukin-8
- RNA, Messenger
- Dexamethasone
- Cyclosporine
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Topics |
- Anti-Inflammatory Agents
(pharmacology)
- Blotting, Northern
- Cells, Cultured
- Chemokine CCL2
(analysis, antagonists & inhibitors)
- Chemokines
(metabolism)
- Cyclosporine
(pharmacology)
- Dexamethasone
(pharmacology)
- Enzyme-Linked Immunosorbent Assay
- Eye Diseases
(genetics, metabolism)
- Fibroblasts
(drug effects, metabolism)
- Humans
- Immunosuppressive Agents
(pharmacology)
- Interleukin-8
(analysis, antagonists & inhibitors)
- RNA, Messenger
(analysis)
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