| Summary: | 碩士 === 國立成功大學 === 微生物暨免疫學研究所 === 95 === The group A streptococcus (GAS) causes a variety of diseases, ranging from mild self-limiting infection to severe life-threatening infection, such as pharyngitis, tonsillitis, and tympanitis to necrotizing fasciitis, bacteremia, and streptococcus toxic shock syndrome (STSS). The disease severity may be associated with the different bacterial serotype or depend on patient’s healthy condition. Previous clinical findings indicated that patients with sepsis had lower level of kallistatin protein. Kallistatin was originally found to be a tissue kallikrein-binding protein. But recent studies have shown that kallistatin may function independently of its interaction with tissue kallikrein. Kallistatin has some biological effects, such as anti-angiogenesis, anti-inflammation, and anti-oxidation and possesses beneficial effects in hypertensive, cardiovascular and renal diseases. However, the effects of kallistatin in microbial infection have not been explored. In this study, we transiently overexpressed kallistatin gene by hydrodynamic injection and investigated the protective effects of kallistatin in a mouse model of GAS infection. We found that kallistatin increased the survival rate of GAS-infected mice. The bacterial numbers and the inflammatory cytokines and chemokines in the local infection site and blood were lower in kallistatin-treated group than those in control groups. In contrast with control mice, kallistatin-treatment decreased neutrophil infiltration into the local infection site, while promoting neutrophil viability. In the histological analysis, the skin and liver tissue showed less damage after treatment with kallistatin compared to the control groups. Consequently, we will examine the biological function and therapeutic effect of kallistatin in GAS-infected mice.
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