No abstract

The sensitizing effect and the local and general toxicity related to membrane components of the archaeobacterium SulJblubus solfatarieus was studied. Celt envelope fragments were biologically active but this activity was lost upon separation of the lipid and protein components. The envelope fragments exerted lethal effects on mice sensitized with D-galactosamine that were prevented by pretreatment with anti-TNF-a serum. This tethal activity occurred in both LPS-responder (BALB/cByJ) and LPS-oonresponder (C3H/HeJ) mouse strains. In addition, Suytlubus envelope fragments tested in rabbits caused a local Shwartzman reaction, and showed pyrogenic activity. In vituo, the envelope fragments that act on spleen lymphocytes of the LPS-responder (BALB/cByJ) and LPSnonresponder (C3H/HeJ) mice caused an uptake of [3H]thymidine similar to that caused by concanavalin A. A similar toxic activity to that exerted by eubacteria is therefore exerted by this non-pathogenic archaeobacterium despite the difference in surface chemistry.

Summary Murine splenocytes treated with prolactin (PRL) or insulin were stimulated in vitro with porins or lipopolysaccharide (LPS) of Salmonella typhimurium. It was seen that PRL inhibits the release of IFN-y from splenocytes treated with porins by about 20% while having no effect on the release of IL-1-a. Splenocytes stimulated with LPS, in the presence of PRL, had a reduced release of IFN-y (35%) and IL-I-a (70%). The porin-stimulated splenocytes exhibited a remarkable increase in IL-l-a release (100%) and a diminished release of IFN-y (about 50%) in the presence of insulin. The splenocytes stimulated with LPS had a reduced release of IL-l-a (75%) and IFN-Y (about 50%) when insulin was added.The data suggest that the classical endocrine system participates in a bioregulatory feedback loop that may prevent unwanted toxicity from cytokine excess. However, some bacterial products sometimes enormously unbalance this regulatory network.

In this study, changes were investigated in release of IL-1alpha, IFN-gamma and IL-4 from mouse splenocytes stimulated with staphylococcal protein A (SpA), toxic shock syndrome toxin-1 (TSST-1) or streptococcal lysin S (SLS) in the presence of insulin. The results show that insulin-treated splenocytes stimulated by SpA had a 25% increase in IFN-gamma release and a 50% decrease in IL-4 compared with splenocytes treated with SpA alone. IL-1alpha release was unchanged compared with controls. Insulintreated splenocytes stimulated with TSST-1 had a 30% fall in IL-1alpha and IFN-gamma release compared with controls. There were no changes in IL-4 release. Splenocytes stimulated with SLS after insulin treatment increased their release of IL-1alpha and IFN-gamma by 50%, whereas IL-4 release was unchanged. The data suggest that the insulin may have important functional implications in immunoregulation.