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[The effects of glucocorticoid on rabbit polymorphonuclears during inflammation]
1Department of Pathophysiology, Second Military Medical University, Shanghai.
Zhonghua Yi Xue Za Zhi
|May 1, 1995
Summary
Glucocorticoids inhibit tumor necrosis factor-induced CD18 expression on rabbit polymorphonuclears (PMNs) via the glucocorticoid receptor (GR). This inhibition correlates with reduced PMN adhesion, highlighting GC
Area of Science:
- Immunology
- Cell Biology
- Pharmacology
Background:
- Tumor necrosis factor (TNF) can increase CD18 expression on polymorphonuclears (PMNs).
- CD18 is crucial for PMN adhesion to ICAM-1.
- Glucocorticoids (GCs) are potent anti-inflammatory drugs.
Purpose of the Study:
- To investigate the effect of glucocorticoids on CD18 expression in rabbit PMNs stimulated by TNF.
- To analyze the correlation between CD18 expression and PMN adhesion rate.
- To determine the role of the glucocorticoid receptor (GR) in this process.
Main Methods:
- Quantification of CD18 expression on rabbit PMNs.
- Measurement of rabbit PMN adhesion to ICAM-1 coated magnetic beads.
- Inhibition of GR using RU 38486.
- Culture of PMNs with varying concentrations of dexamethasone (Dex).
Main Results:
- TNF increased CD18 expression on rabbit PMNs.
- Glucocorticoid treatment inhibited the TNF-induced rise in CD18 expression.
- Blocking the glucocorticoid receptor (GR) with RU 38486 reversed the inhibitory effect of GCs.
- A positive correlation (r = 0.966) was observed between CD18 expression and PMN adhesion rate after dexamethasone treatment.
- GCs were found to inhibit PMN adhesion.
Conclusions:
- Glucocorticoids inhibit TNF-induced CD18 expression on rabbit PMNs.
- This inhibition is mediated by the glucocorticoid receptor (GR).
- GCs play a significant role in inhibiting PMN adhesion, likely through modulation of CD18 expression.