| Summary: | 碩士 === 慈濟大學 === 分子生物暨人類遺傳學研究所 === 98 === Anthrax, a disease caused by Bacillus anthracis infection, causes animal and human death through unknown mechanisms. Lethal toxin (LT), a mitogen-activated protein kinase kinase (MAPKKs) inhibitor, is the major virulence factor of B. anthracis. LT treatments cause lethality and certain anthrax-like pathogenesis of experimental mice, including hypoxic tissue damages and anemia. One literature reported that LT-induced in vitro hemolysis plays certain roles. Our previous studies indicated that LT could block erythroid differentiation in vitro and in vivo. Since granulocyte-colony stimulating factor (G-CSF) is a pleiotropic cytokine playing a major role as a regulator of hematopoiesis and has the ability to protect cells from apoptosis. These prompt us to analyze whether treatments of G-CSF could ameliorate LT-induced anemia and lethality. Our data showed that G-CSF treatments reduced LT-mediated mortality is associated with amelioration of reduced anemia response. We also demonstrated that LT induced anemia is not due to hemolysis, in addition, G-CSF pretreatments could ameliorate LT induced erythropoiesis suppression.
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