Modulation Of TNF Alpha And IL-1 Beta From Endotoxin-stimulated ...

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Abstract

The effect of selective PDE isozyme inhibitors including vinpocetine (PDE-I), CI-930 and milrinone (PDE-III), rolipram and nitraquazone (PDE-IV) and zaprinast (PDE-V) on monocyte viability and production of tumor necrosis factor (TNF alpha) and interleukin-1 beta (IL-1 beta) elicited from endotoxin-stimulated human monocytes was investigated. None of the inhibitors affected monocyte viability at 10 microM or lower concentrations. PDE-IV inhibitors and to a lesser extent, PDE-III inhibitors suppressed TNF alpha production. Only high concentrations of PDE-IV inhibitors modestly suppressed IL-1 beta. Zaprinast stimulated IL-1 beta and to a lesser extent TNF alpha production. These data show that TNF alpha and IL-1 beta production are differentially regulated, and that PDE III, PDE-IV and PDE-V isozymes are functional in endotoxin-stimulated monocytes. Clinical trials will be needed to ascertain if PDE-IV inhibitors are able to suppress TNF alpha levels in man.

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References

1. 1. Annu Rev Immunol. 1989;7:625-55 - PubMed
2. 1. Mol Cell Biol. 1990 Jun;10(6):2678-86 - PubMed
3. 1. J Immunol. 1988 Oct 1;141(7):2388-93 - PubMed
4. 1. J Immunol Methods. 1983 Dec 16;65(1-2):55-63 - PubMed
5. 1. J Allergy Clin Immunol. 1992 May;89(5):958-67 - PubMed

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