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Histamine induces interleukin-8 secretion by endothelial cells
P Jeannin1, Y Delneste, P Gosset
1Pathologie Immuno-Allergique Respiratoire et Cellules Inflammatoires, INSERM U-416, Institut Pasteur, Lille, France.
Blood
|October 1, 1994
Summary
Histamine stimulates endothelial cells to produce interleukin-8 (IL-8), a key mediator in late-phase allergic inflammation. This finding reveals a novel role for histamine in controlling delayed inflammatory responses.
Area of Science:
- Endocrinology
- Immunology
- Cell Biology
Background:
- Histamine triggers early endothelial cell (EC) responses like P-selectin expression and mediator release.
- Delayed effects of histamine on EC, particularly cytokine production, remain largely uncharacterized.
Purpose of the Study:
- To investigate the impact of histamine on interleukin-8 (IL-8) production by endothelial cells.
- To elucidate the mechanisms and kinetics of histamine-induced IL-8 expression in EC.
Main Methods:
- Enzyme-linked immunosorbent assay (ELISA) to quantify IL-8 secretion.
- Messenger RNA (mRNA) expression analysis to assess IL-8 gene regulation.
- Dose-response studies and receptor antagonist inhibition assays.
Main Results:
- Histamine significantly increased both IL-8 secretion and mRNA expression in EC.
- The effect was dose-dependent, requiring concentrations greater than or equal to 10(-6) mol/L.
- IL-8 production was potentiated by co-stimulation with tumor necrosis factor-alpha (TNF-alpha).
- Histamine-induced IL-8 production was inhibited by H1 or H2 receptor antagonists.
- Elevated IL-8 levels were observed starting 4 hours post-stimulation, indicating a delayed effect.
Conclusions:
- Histamine plays a role in the late inflammatory phase of allergic disorders.
- Histamine promotes IL-8 secretion by endothelial cells, contributing to delayed inflammatory reactions.
- Targeting histamine receptors may offer therapeutic strategies for managing allergic inflammation.