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Volume 270, Number 10, Issue of March 10, 1995 pp. 5084-5088
©1995 by The American Society for Biochemistry and Molecular Biology, Inc.
Interleukin-13 Inhibits Protein Kinase C-triggered Respiratory Burst in Human Monocytes
ROLE OF CALCIUM AND CYCLIC AMP

(Received for publication, October 3, 1994; and in revised form, December 9, 1994)

Patricia Sozzani Claudie Cambon Natalio Vita Marie-Hélène Séguélas Daniel Caput Pascual Ferrara Bernard Pipy

Interleukin-13 (IL-13), a novel cytokine produced by activated lymphocytes modulates some monocyte functions, but no data is available concerning the signal transduction pathway. We show here, the inhibitory effect of IL-13 on 12-O-tetradecanoylphorbol-13-acetate (TPA)-triggered reactive oxygen intermediate production in human monocytes and the signals involved in this response. Our results show that IL-13 produces rapid and transient phosphoinositide hydrolysis and intracellular Ca mobilization. Furthermore, IL-13 induces intracellular cAMP accumulation through inositol 1,4,5-trisphosphate-dependent Ca mobilization. Metabolic inhibitors were used to relate the first steps in signaling pathways to the inhibitory effect of IL-13 on TPA-triggered reactive oxygen intermediate production. Indeed, inhibitors of phospholipase C (neomycin), intracellular Ca mobilization (8-[N,N-diethylamino]-octyl 3,4,5-trimethoxybenzoate hydrochloride), adenylate cyclase (Delta^9-tetrahydrocannabinol), and protein kinase A (N-[2-(p-bromocinnamylamino)ethyl]-5-isoquinolinesulfonamide) impair the IL-13 inhibitory response. Altogether these observations indicate that modulatory effect of IL-13 on the TPA-induced oxidative burst is the result of the intracellular cAMP accumulation through an inositol 1,4,5-trisphosphate-induced Ca mobilization-dependent pathway.




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