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Complexes of polyadenylic and polyuridylic acids, or of polycytidylic acid and methylated bovine serum albumin, enhance the early rate of increase in numbers of antibody-forming spleen cells in mice immunized with sheep red blood cells or other particulate antigens. Polyadenylic and polycytidylic acids, respectively, appear to be the source of the critical stimulators which, as demonstrated by others in bacteria, may act by influencing nucleotide kinase activity. The stimulated antibody response, but not the normal response, is antagonized by kinetin riboside and by an adenosine derivative occurring in sRNA.

Enterobacteriaceae and oral black-pigmented bacteria (Porphyromonas gingivalis and Prevotella intermedia) are known to activate LPS-refractory C3H/HeJ macrophages. When contaminating proteins are removed from R-form LPS of Enterobacteriaceae by repurification, however, this ability is lost. In the present study, we investigated the capacity of LPS from P. gingivalis, P. intermedia, Salmonella minnesota, and Salmonella abortusequi to induce production of tumor necrosis factor (TNF) in gamma interferon-primed C3H/HeJ macrophages before and after repurification. P. abortusequi S-LPS was fractionated by centrifugal partition chromatography into two LPS forms: SL-LPS, having homologous long O-polysaccharide chains, and SS-LPS having short oligosaccharide chains. Prior to repurification, all LPS forms except SL-LPS induced TNF production in both C3H/HeJ and C3H/HeN macrophages. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis showed that repurification removed contaminating protein from the preparations, and repurified SS-LPS and S. minnesota Ra-LPS no longer stimulated TNF production in C3H/HeJ macrophages, although C3H/HeN macrophages remained responsive. In contrast, repurified oral bacterial LPS retained the capacity to induce TNF production in C3H/HeJ macrophages. Oral bacterial LPS preparations also were not antagonized by excess inactive, repurified SL-LPS; Ra-LPS; Rhodobacter sphaeroides lipid A, a competitive LPS antagonist, or paclitaxel, an LPS agonist, and they were comparatively resistant to polymyxin B treatment. Nevertheless, oral bacterial LPS was less toxic to D-galactosamine-treated C3H/HeN mice than was LPS from Salmonella. These findings indicate that the active molecule(s) and mode of action of LPS from P. gingivalis and P. intermedia are quite different from those of LPS from Salmonella.

Toxicity of the cells of a newly established axenic Microcystis aeruginosa K-139 strain to mice was studied. LD50 of the cells harvested in the mid-log phase was 7.3mg/kg. The organs of acute dead mice were examined histopathologically.The blood congestion and necrosis of the parenchymal cells around the central veins in the liver were observed, but other organs seemed to be normal. The liver damage was confirmed by the tests of glutamic oxaloacetic transaminase (GOT) and glutamic pyruvic transaminase (GPT) activities in the sera of the mice after the injection with the K-139 cells. Furthermore, the K-139 cells were capable of inducing interleukin 1 (IL-1) production by peritoneal macrophages in vitro.Cyanobacteria (blue-green algae) belonging to the genus Microcystis were mostly responsible for the development of massive surface blooms in eutrophic waters (4, 6). Water pollution by Microcystis and other cyanobacteria is becoming a serious problem in many countries, including Japan. Natural cases of poisoning of large domestic animals by the blue-green alga Microcystis aeruginosa are not uncommon (3,4,6). Some strains and blooms of Microcystis were reported to contain toxins (1,3,4,(6)(7)(8)13). The toxins produced by M. aeruginosa are a related family of cyclic heptapeptides with molecular weights ranging from 909 to 1,044 (2). These toxins had cytotoxic properties which caused extensive hemorrhage in the liver (5,8,13). Lake Kasumigaura in Ibaraki prefecture has such blooms especially in summer, and M. aeruginosa is the most dominant alga in this lake. In a previous paper (12), we demonstrated that there were toxic and non-toxic algal blooms consisting of Microcystis grown in Lake Kasumigaura, and the mice that had received nontoxic Microcystis showed delayed-type hypersensitivity after the injection of specific antigen. Since Microcystis organisms form mucilaginous colonies and some bacteria are usually tightly associated with the colonies, isolation of axenic strains from the colonies is very difficult. However, we have succeeded in isolating them by developing a solid media suitable for the growth of Microcystis species (manuscript in preparation). In the present study, we deal with the toxicity of a newly established 787

Abstract:The present study deals with whether lipopolysaccharide