An examination of the immune system of the duck (Anas platyrhynchos) for factors resembling some defined mammalian cytokines.

Duck lymphoblasts generated by phytohaemagglutinin (PHA) did not respond to recombinant or Jurkat cell line human interleukin (IL)-2 or possess surface antigens resembling mammalian IL-2 receptors or IL-1 beta. Supernatant fluids from normal and PHA-stimulated duck lymphocyte cultures, and normal and lipopolysaccharide (LPS)-stimulated monocytes, gave negative results in a range of assays for biological activity and immunochemical presence of factors resembling mammalian IL-1 and IL-2. However, supernatant fluids from LPS-stimulated duck monocytes contained IL-6-like activity (up to 35 units/mL) assessed on the 7TD-1 murine cell line.

Production of cytokines (TNF-alpha, IL-1-beta) and endothelial cell activation in human liver allograft rejection.

Intragraft production of tumor necrosis factor-alpha (TNF-alpha) and interleukin-1-beta (IL-1-beta) was determined in rejecting human liver grafts during acute rejection and in chronic graft dysfunction. The localization of cytokine-producing cells was then correlated with the distribution of monocytes and macrophages as their main producers, as well as with effector functions such as endothelial cell activation. In selected patients collateral TNF-alpha plasma levels were measured.

Modulation of lipopolysaccharide-induced production of tumor necrosis factor, interleukin 1, and interleukin 6 by synthetic precursor Ia of lipid A.

Endotoxin (lipopolysaccharide, LPS) induces the production of mediators of inflammation, which exerts pathophysiological effects such as fever or shock in mammals. In the present study we have investigated the modulation of LPS by the synthetic non-active tetraacylated precursor Ia of lipid A (compound 406) in the induction of tumor necrosis factor (TNF), interleukin 1 (IL-1) and interleukin 6 (IL-6) in human peripheral blood mononuclear cells (PBMC) and in human peripheral blood monocytes (PBMo). PBMC stimulated with LPS released TNF in a concentration dependent manner.

Suppressive effect of lipid A partial structures on lipopolysaccharide or lipid A-induced release of interleukin 1 by human monocytes.

Experiments were designed to investigate the significance of lipid A partial structures, precursor Ia (compound 406), and lipid X (compound 401) to serve as antagonists of interleukin 1 (IL-1) release from human mononuclear cells and monocytes induced by lipopolysaccharide (LPS, endotoxin) of Salmonella abortus equi or synthetic Escherichia coli lipid A (compound 506). A definite inhibition mediated by lipid A partial structures on IL-1 release induced by LPS or lipid A was found in repeated experiments. The inhibitory effect was exerted not only on IL-1 release, but also on IL-1 peptide synthesis at the intracellular level.

Functional and molecular characterization of a monoclonal antibody against the 165-186 peptide of human IL-1 beta.

A synthetic peptide of human recombinant interleukin 1 beta (hrIL-1 beta) 165-186, which exhibits biological activity in the human fibroblast assay, was used as an immunizing antigen to obtain a murine monoclonal antibody (MoAb) termed FIB 1. This MoAb, an IgG1, reacts specifically with hrIL-1 beta, but not with hrIL-1 alpha, as measured in enzyme-linked immunosorbent assays (ELISA). The MoAb FIB 1 detects the characteristic 17 kDa IL-1 protein in Western blots.

Detection of interleukin 1 with human dermal fibroblasts.

A fibroblast proliferation assay was developed for the detection of interleukin 1 (IL 1). Proliferation was measured by thymidine incorporation and by staining of cellular proteins with crystal violet. Response of fibroblasts was optimal at cell numbers of 4,000 to 9,000 cells/culture and an incubation period of four days.

Immunoenzymatic assessment of IL-1 beta mRNA by in situ hybridization using sulphonated probes.

An immunoenzymatic detection method of in-situ hybridization reactions for interleukin 1 (IL-1) beta was established, using sulphonated probes. As model system we used unstimulated and lipopolysaccharide (LPS) stimulated peripheral blood mononuclear cells (PBMNC). After hybridization, sulphone groups were targeted with a monoclonal antibody, and bound antibody was visualized by the alkaline phosphatase anti-alkaline phosphatase (APAAP) method.