title: [Prostaglandin E2 and interleukin-1-producing activity of plastic-adherent cells from cancer patients as a result of modification by BRM therapy].
abstract: It is crucial to define the immunological characteristics of peripheral blood mononuclear cells in order to clarify the physiological state of cancer patients. In this study, we examined prostaglandin E2 (PGE2) and interleukin-1 (IL-1) production by plastic-adherent cells stimulated by lipopolysaccharide (LPS). The secretion of PGE2 and IL-1 into media depended on the dose of LPS. Although the addition of silica resulted in suppression of LPS-induced PGE2 production, it caused augmentation of IL-1 production. The effect of BRM therapy on IL-1 production was evaluated in five cancer patients. The results demonstrated that BRM therapy increased the levels of IL-1 at the late assessment point for 3 patients and their quality of life was improved. These findings suggest that production of IL-1 may be used as a monitor for the effectiveness of biotherapy. The association of PGE2 production with host antitumor response was evaluated in IFN-gamma therapy. The results showed that the PGE2 production ratio increased early in the therapy period and declined gradually, whereas the expression of HLA-DR antigen on monocytes and the level of IL-1 increased during the treatment. The exact mechanism by which BRM activates monocytes is unknown. It is possible that a distinct subpopulation of monocytes is responsible for this effect.
mesh_terms: D001688:Biological Products / Q000627:therapeutic use*; D002448:Cell Adhesion; D002478:Cells, Cultured; D003110:Colonic Neoplasms / Q000276:immunology / Q000628:therapy; D015232:Dinoprostone; D006801:Humans; D007375:Interleukin-1 / Q000096:biosynthesis*; D008070:Lipopolysaccharides / Q000494:pharmacology; D008175:Lung Neoplasms / Q000276:immunology / Q000628:therapy; D008264:Macrophages / Q000276:immunology / Q000378:metabolism; D009000:Monocytes / Q000276:immunology / Q000378:metabolism*; D009369:Neoplasms / Q000276:immunology / Q000628:therapy*; D010844:Picibanil / Q000627:therapeutic use*; D011458:Prostaglandins E / Q000096:biosynthesis*; D013274:Stomach Neoplasms / Q000276:immunology / Q000628:therapy
chemical_list: D001688:Biological Products; D007375:Interleukin-1; D008070:Lipopolysaccharides; D011458:Prostaglandins E; D010844:Picibanil; D015232:Dinoprostone