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

Chemotactic factors regulate the recruitment of neutrophils, lymphocytes, or monocytes-macrophages to infectious and inflammatory sites. The purpose of this study was to determine whether monocyte-chemotactic and -activating factor (MCAF [MCP-1I, aJE gene product) also influences the host defense mechanism against microbial infection. We evaluated the effect of recombinant human MCAF on the survival rate of mice systemically infected with Pseudomonas aeruginosa or Salmonella typhimurium. The administration of 2.5 ,ug of MCAF 6 h before infection completely protected the mice from lethal infection. Mice with cyclophosphamideinduced leukopenia exhibiting increased susceptibility to P. aeruginosa were also endowed with resistance by the same dose of MCAF. Administration of MCAF at -6 h was critical, since MCAF given either earlier or later than -6 h failed to rescue mice from lethal infection. The in vivo effect on the survival of mice paralleled the reduced recovery of viable P. aeruginosa or S. typhimurium from the peritoneal cavity, i.e., the number of recovered bacteria from the MCAF (2.5 ,ug per mouse)-treated mice was reduced to less than 2% of control mice for P. aeruginosa and 4% of control mice for S. typhimurium at 24 h. Since MCAF exhibited chemotaxis on murine macrophages as well as enhanced phagocytosis and killing of bacteria in vitro, the activation of macrophages, followed by the recruitment into the peritoneal cavity, is responsible for eliminating bacteria and thus enhancing the survival rate.

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