Sriskandan S, Moyes D, Buttery L K, Krausz T, Evans T J, Polak J, Cohen J
Department of Infectious Diseases and Bacteriology, Royal Postgraduate Medical School, Hammersmith Hospital, London, United Kingdom.
J Infect Dis. 1996 Jun;173(6):1399-407. doi: 10.1093/infdis/173.6.1399.
The role of streptococcal pyrogenic exotoxin A (SPEA) was evaluated in a murine model of fasciitis and multiorgan failure due to a toxigenic strain of Streptococcus pyogenes. Increased serum levels of SPEA at 15 and 21 h were associated with a survival time of <24 h. Levels of SPEA correlated with interleukin-6 levels. Immunostaining showed SPEA localized to renal and hepatic cells. Neutralizing rabbit antibody to SPEA was administered to mice challenged with S. pyogenes, but no effect on survival was observed. Vaccination of mice with recombinant SPEA enhanced mortality due to streptococcal infection, despite the development of neutralizing immunity to the toxin prior to infection. Hence, SPEA is produced systemically during S. pyogenes soft-tissue infection, and increased levels are associated with reduced survival. In this model, however, SPEA did not appear to play a dominant role in pathogenesis; passive immunization against SPEA was not protective, and active immunization enhanced mortality.
在由产毒素的化脓性链球菌菌株引起的筋膜炎和多器官衰竭小鼠模型中,对化脓性链球菌致热外毒素A(SPEA)的作用进行了评估。在15小时和21小时时血清SPEA水平升高与生存时间<24小时相关。SPEA水平与白细胞介素-6水平相关。免疫染色显示SPEA定位于肾细胞和肝细胞。将抗SPEA的中和兔抗体给予感染化脓性链球菌的小鼠,但未观察到对生存有影响。用重组SPEA对小鼠进行疫苗接种,尽管在感染前已产生对该毒素的中和免疫,但却增加了链球菌感染导致的死亡率。因此,在化脓性链球菌软组织感染期间,SPEA在全身产生,其水平升高与生存率降低相关。然而,在该模型中,SPEA似乎在发病机制中不发挥主导作用;针对SPEA的被动免疫没有保护作用,而主动免疫则增加了死亡率。