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* Laboratoire d’Immunologie and Unité INSERM 479, Hôpital Bichat, and
Département d’Anesthésie-Réanimation, Hôpital Saint-Louis, Paris, France
Correspondence: Dr. Sylvie Chollet-Martin, Laboratoire d’Immunologie et Unité INSERM 479, Hôpital Bichat, 46 rue Henri Huchard, 75018 Paris, France. E-mail: sylvie.martin{at}bch.ap-hop-paris.fr
Interleukin (IL) 12 is a heterodimeric cytokine mainly produced by
phagocytes—important target cells for IL-12 in particular with a
chemotactic effect—and antigen-presenting cells in response to various
microorganisms. Because IL-8 is a strong chemokine for
polymorphonuclear neutrophils (PMNs), we investigated the effect of
IL-12 on PMN IL-8 production. IL-12 alone had no significant effect,
but with lipopolysaccharide (LPS) it was additive at both protein and
mRNA levels. Actinomycin D at the beginning of culture inhibited IL-8
mRNA induction, whereas late addition affected IL-8 transcript
stability, suggesting gene transcription involvement. Results with
parthenolide and tyrphostin AG490 suggest that nuclear factor-
B and
signal transducer and activator of transcription 4 play a role. The
IL-12 additive effect was restricted to IL-8 release, with no action on
cell-associated IL-8. IL-12 additive effects occurred after 18 h
of culture, with no marked up-regulation of IL-12 receptor expression,
and were blocked by actinomycin D added after 16 h of culture.
Tumor necrosis factor (TNF) 
and interferon (IFN) 
had
intermediate roles; their specific inhibition reduced IL-12’s effect.
IL-12’s chemotactic mechanism seemed mediated by overproduction and
release of IL-8 by human PMNs in the presence of LPS, an effect
involving TNF- and IFN- secretion. These results point to a new
role for IL-12 in inflammation, through an autocrine amplification
loop.
Key Words: phagocyte • chemokine • mRNA • inflammation
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