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| Item Type: | Article |
|---|---|
| Title: | beta-adrenergic receptor stimulation selectively inhibits IL-12p40 release in microglia |
| Creators Name: | Prinz, M., Haeusler, K.G., Kettenmann, H. and Hanisch, U.K. |
| Abstract: | The cytokine interleukin-12 (IL-12) is mainly produced in response to bacterial or parasitic infections. We examined the capacity of mouse brain microglia to release IL-12 forms upon challenge with bacterial lipopolysaccharide (LPS) and studied its modulation by sympathomimetics. LPS evoked the release of IL-12p40 whereas the heterodimeric form, IL-12p70 was virtually undetectable. Sympathomimetics such as salbutamol dose-dependently inhibited IL-12p40 release, whereas the production of IL-6, TNF{alpha} and MIP-1α was only marginally influenced. The inhibitory effect of salbutamol could be abolished by {beta}-antagonists, such as oxprenolol. The cAMP-elevating agent forskolin could mimic the effects of {beta}-agonists, indicating that IL-12p40 release inhibition involves intracellular cAMP accumulation. While microglial IL-12p40 may play a role in the regulation of IL-12p70 bioactivity, microglial release is itself modulated by IL-12p70. Recombinant IL-12p70 was found to enhance the LPS-evoked release of MIP-1α and to have a biphasic effect on both TNFα and MIP-1{alpha} with release augmentation at lower and attenuation at higher doses. Finally, no functional correlation was found between the release of IL-12p40 and the induction of Kv1.3 potassium channels, another marker of microglial activation. Taken together, {beta}2-adrenoreceptor-mediated effects on microglial cyto- and chemokine release via cAMP accumulation could modulate inflammatory cascades during bacterial infections. |
| Keywords: | {Beta}2-Adrenoreceptor, Chemokines, Cytokines, Kv1.3, Margatoxin, Salbutamol |
| Source: | Brain Research |
| ISSN: | 0006-8993 |
| Publisher: | Elsevier |
| Volume: | 899 |
| Number: | 1-2 |
| Page Range: | 264-270 |
| Date: | 1 January 2001 |
| PubMed: | View item in PubMed |
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