Fig. 6.

Mediator implicated in the inhibition of alveolar macrophage (AM) macrophage inflammatory protein-1α (MIP-1α) production by 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK). AMs were treated with NNK (500 µM), alone or together with NS-398 (10 µM), indomethacin (10 µM) or anti-prostaglandin E₂ (anti-PGE₂) antibody (dilution 1 : 25), or with PGE₂ (25 ng/ml) without lipopolysaccharide (LPS), for 20 h. Cell-free supernatants were analysed for MIP-1α content. COX inhibitors and anti-PGE₂ antibody abrogated the inhibitory effect of NNK on MIP-1α release by AMs (no significant inhibition). NNK and exogenous PGE₂ significantly (*P < 0·005) inhibited AM MIP-1α release.