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(Journal of Leukocyte Biology. 2002;72:995-1002.)
© 2002 by Society for Leukocyte Biology

IL-12-dependent nuclear factor-B activation leads to de novo synthesis and release of IL-8 and TNF- in human neutrophils

Department of Biological and Medical Research, King Faisal Specialist Hospital and Research Centre, Riyadh, Saudi Arabia

Correspondence: Futwan Al-Mohanna, Biological and Medical Research Department, MBC 03, King Faisal Specialist Hospital and Research Centre, Riyadh 11211, Saudi Arabia. E-mail: Futwan{at}kfshrc.edu.sa

The cytokine interleukin (IL)-12 plays a bridging role between innate and adaptive immunity. Here, we demonstrate that treatment of neutrophils with IL-12 leads to a transient increase in intracellular-free calcium [Ca⁺⁺]_i levels, which is necessary for the production of reactive oxygen metabolites (ROM). This production is associated with the activation and nuclear translocation of the transcription factor nuclear factor (NF)-B and is inhibited in the presence of the intracellular calcium chelator 1,2-bis(O-amminophenoxy) ethane-N,N-N',N'-tetraacetic acid-acetoxymethyl ester and the ROM production inhibitor diphenyl iodonium. We show that IL-12 causes a significant increase in total mRNA levels, which appear dependent on the generated ROM. In addition IL-12 induces the de novo synthesis and production of IL-8 and tumor necrosis factor (TNF-) in a calcium- and ROM-dependent manner. Our data demonstrate a direct role for IL-12 in the activation of human neutrophils and suggest a ROM-dependent interplay between IL-12-induced [Ca⁺⁺]_i transient and the release of IL-8 and TNF- through NF-B activation.

Key Words: calcium • diphenylene iodonium • neutrophils

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