Protective Role of Peroxiredoxin I in Heat-Killed Staphylococcus Aureus-infected Mice

过氧化物酶 I 在热灭活金黄色葡萄球菌感染小鼠中的保护作用

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作者:Hu-Nan Sun #, Yue Liu #, Jian-Nan Wang, Chuang Wang, Ren Liu, Ling-Zu Kong, Xing Zhen, Nisansala Chandimali, Yu-Dong Cui, Sun-Uk Kim, Dong-Seok Lee, Dae-Yeul Yu, Ji-Su Kim, Dong Kee Jeong, Taeho Kwon, Ying-Hao Han

Aim

Staphylococcus aureus (S. aureus) is a major gram-positive pathogen, which can cause toxic and immunogenic injuries both in nosocomial and community-acquired infections. Peroxiredoxin (Prx) I plays crucial roles in cellular apoptosis, proliferation, and signal transduction as well as in immunoregulation. The present study aimed to investigate whether Prx I protects mice from death caused by the heat-killed Staphylococcus aureus. Materials and

Conclusion

Enhanced mortality of S. aureus-infected mice with Prx I deficiency suggested that Prx I may protect against the infection-associated lethality of mice.

Methods

In the present study, we challenged the wild-type and Prx I-deficient mice with heat-killed S. aureus (HKSA). The effects of Prx I were evaluated by a series of in vitro and in vivo experiments including western blot, Haematoxylin and Eosin staining, splenocyte analysis and cytokines analysis.

Results

Intra-peritoneal (ip) inoculation of HKSA resulted in increased mortality of Prx I-knockout (KO) mice with severe liver damage and highly populated spleens with lymphocytes. Furthermore, HKSA infections also bursted the production of both pro-inflammatory and anti-inflammatory serum cytokines in Prx I KO compared to wild-type mice.

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