| Summary: | The effect of the addition of leucocytes or leucocyte supernatants on the turbot macrophage respiratory burst was determined. When macrophages and leucocytes were co-incubated, the highest suppressive effect on the respiratory burst was found after 24 h. The addition of turbot leucocyte's supernatants from cells cultured for 17 h with culture media and foetal calf serum, to macrophage monolayers from the same or different animals resulted, in both cases, in the inhibition of the macrophage respiratory burst. Leucocyte supernatants also suppressed PHA-induced proliferation of blood lymphocytes. Inhibitors of the two main pathways of eicosanoid biosynthesis, the cyclooxygenase and lipoxygenase pathways, were also used to obtain supernatants. Although both resulting supernatants restored the macrophage respiratory burst activity, only cyclooxygenase derived products seemed to be implicated in the suppressive effect on macrophage respiratory burst. Nordihydroguaiaretic acid (NDGA), an inhibitor of lipoxygenase activity, was able to restore lymphocyte proliferation to normal levels (1:2 dilution), suggesting that eicosanoids derived from lipoxygenase can be related to the inhibition of the PHA-induced proliferation. © 1999 Academic Press. Peer Reviewed
|
|---|