[IL-1, TNF and IL-6 production by alveolar mononuclear cells in patients with sarcoidosis]. / Stvaranje interleukina-jedan, faktora nekroze tumora i interleukina-sest od strane alveolnih mononuklearnih celija kod bolesnika sa sarkoidozom pluca.

Cytokines produced by locally activated T cells and macrophages have central role in lymphocyte alveolitis and granuloma formation, and it is beleived that they regulate activity and further progression of sarcoidosis. The aim of our study was to evaluate the levels of interleukin-1 (IL-1), tumor necrosis factor (TNF) and interleukin-6 (IL-6) production by bronchoalveolar mononuclear cells in 6 patients With sarcoidosis. The obtained results showed increased IL-6 levels in patients with active disease, IL-1 activity did not follow clinical changes, while TNF was detectible only in one patients.

Interleukin-1 in vivo modulates trauma-induced immunosuppression.

To elucidate the mechanisms underlying trauma-induced immunosuppression and decreased IL-2 production we evaluated: 1) the effect of trauma on IL-1 production at different time intervals and 2) the effect of IL-1 in vivo administration on immune functions (IL-1 production, IL2 production, NK cell cytotoxicity) in normal and traumatized mice. Experiments were performed on CBA/H mice a) subjected to scald injury (sacrificed 3 h and 6 h later) b) treated with IL-1 in vivo (human recombinant IL-1 beta 100 ng/mouse, sacrificed 21 h and 24 h later) and c) subjected to both IL-1 in vivo treatment and scald (IL-1 was given 18 h before scald, animals were sacrificed 3 h and 6 h after scald i.e. 21 h and 24 h after IL-1 administration). Our results demonstrate that trauma alone increases IL-1 production from 1 h to 24 h after trauma infliction. Recombinant IL-1 given in vivo also induces a significant rise in IL-1 production. When mice were subjected to both trauma and IL-1 in vivo treatment, the rise in IL-1 production was not additive. Trauma induced severe depression of IL-2 production which could not be overcome by in vitro addition of IL-1 to IL-2 producing splenocytes from traumatized mice. In contrast, IL-1 administered in vivo stimulated IL-2 production in normal mice, and when given prior to trauma infliction, it completely abrogated trauma-induced suppression of IL-2 production. The same effect was seen on NK cell cytotoxicity (an IL-2 dependent function).(ABSTRACT TRUNCATED AT 250 WORDS)