| Summary: | 碩士 === 慈濟大學 === 分子生物及細胞生物研究所 === 96 === Anthrax, a disease caused by Bacillus anthracis infection, usually coincides with hypoxic tissue damages, anemia and lethality; the mechanism associated with its high mortality is not yet clear. Lethal toxin is the major virulent factor of B. anthracis, which was found to be a mitogen-activated protein kinase kinase (MAPKKs) inhibitor. Treatments of lethal toxin to experimental mice could reproduce certain anthrax-like pathogenic responses in vivo; this made it an idea molecular tool to study anthrax-mediated pathogenesis. Since anemia and hypoxic tissue damages are involved in anthrax-mediated mortality, these observations prompt us to further analyze whether lethal toxin could influence erythropoiesis. According to our experiments, we found that treatments of lethal toxin indeed inhibit proliferation of human erythro/megakaryocytic cell line (HEL and K562), decreased the number and size of erythroid colonies in mouse colony-forming cell (CFC) assay, and change the percentage of erythroblasts in mouse. In addition, pretreatments of erythropoietin (EPO) significantly ameliorate the mortality of lethal toxin-treated mice. Our data might suggest a new model that lethal toxin primarily blocks erythropoiesis and then causes anemia, hypoxic tissue damages and death.
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