[ODP-170] 免疫不全マウスを用いた新たな劇症型溶血性レンサ球菌感染症マウスモデルの開発
Background: Streptococcal toxic shock syndrome (STSS) is caused by the S. pyogenes infection. It starts with necrotic fasciitis, which rapidly progresses sepsis leading to become acute respiratory distress syndrome (ARDS), multiorgan failure (MOF) and death. The mechanism of STSS has not yet been clear due to a lack of precise animal model.
Methods and results: We previously reported an STSS-like mouse model using ddY with intramuscularinjection of S. pyogenes SP2 strain that caused delayed death after about 20 days along with a rapid weight loss (Saito M. et al., Microbiol Immunol, 2001). In this study, we improved our STSS model using immunocompromised NOD-SCID mice with our method. The NOD-SCID STSS model showed shorter survival period and fasciitis development than ddY model. Histopathological features from multiple tissues will be presented.
Discussion: NOD-SCID mouse lacks T and B cells, thus representing immunocompromised humans. Also, some immunocompromised patients are known to develop STSS that the NOD-SCID STSS model serves as a good model to study the mechanism of STSSdevelopment. The pathogenic factor of SP2 strain involves two-transcription factor component system covR/covS gene mutations (Otsuji K et al., Microb Pathog, 2020). We are now planning covR/covS knockout SP2 infection using NOD-SCID, that may clarify the mechanism of STSS onset.
Methods and results: We previously reported an STSS-like mouse model using ddY with intramuscularinjection of S. pyogenes SP2 strain that caused delayed death after about 20 days along with a rapid weight loss (Saito M. et al., Microbiol Immunol, 2001). In this study, we improved our STSS model using immunocompromised NOD-SCID mice with our method. The NOD-SCID STSS model showed shorter survival period and fasciitis development than ddY model. Histopathological features from multiple tissues will be presented.
Discussion: NOD-SCID mouse lacks T and B cells, thus representing immunocompromised humans. Also, some immunocompromised patients are known to develop STSS that the NOD-SCID STSS model serves as a good model to study the mechanism of STSSdevelopment. The pathogenic factor of SP2 strain involves two-transcription factor component system covR/covS gene mutations (Otsuji K et al., Microb Pathog, 2020). We are now planning covR/covS knockout SP2 infection using NOD-SCID, that may clarify the mechanism of STSS onset.