1. Academic Validation
  2. The Barrier Disruption and Pyroptosis of Intestinal Epithelial Cells Caused by Perfringolysin O (PFO) from Clostridium perfringens

The Barrier Disruption and Pyroptosis of Intestinal Epithelial Cells Caused by Perfringolysin O (PFO) from Clostridium perfringens

  • Cells. 2024 Jul 3;13(13):1140. doi: 10.3390/cells13131140.
Zhankui Liu 1 2 3 4 Shuang Mou 1 2 3 4 Liang Li 1 2 3 4 Qichao Chen 1 2 3 4 Ruicheng Yang 1 2 3 4 Shibang Guo 1 2 3 4 Yancheng Jin 1 2 3 4 Lixinjie Liu 1 2 3 4 Tianzhi Li 1 2 3 4 Huanchun Chen 1 2 3 4 Xiangru Wang 1 2 3 4
Affiliations

Affiliations

  • 1 National Key Laboratory of Agricultural Microbiology, College of Veterinary Medicine, Huazhong Agricultural University, Wuhan 430070, China.
  • 2 Key Laboratory of Preventive Veterinary Medicine in Hubei Province, The Cooperative Innovation Center for Sustainable Pig Production, Wuhan 430070, China.
  • 3 Engineering Research Center of Animal Biopharmaceuticals, The Ministry of Education of the People's Republic of China (MOE), Wuhan 430070, China.
  • 4 Frontiers Science Center for Animal Breeding and Sustainable Production, Wuhan 430070, China.
Abstract

Clostridium perfringens (C. perfringens), a Gram-positive bacterium, produces a variety of toxins and extracellular Enzymes that can lead to disease in both humans and Animals. Common symptoms include abdominal swelling, diarrhea, and intestinal inflammation. Severe cases can result in complications like intestinal hemorrhage, edema, and even death. The primary toxins contributing to morbidity in C. perfringens-infected intestines are CPA, CPB, CPB2, CPE, and PFO. Amongst these, CPB, CPB2, and CPE are implicated in Apoptosis development, while CPA is associated with cell death, increased intracellular ROS levels, and the release of the inflammatory factor IL-18. However, the exact mechanism by which PFO toxins exert their effects in the infected gut is still unidentified. This study demonstrates that a C. perfringens PFO toxin Infection disrupts the intestinal epithelial barrier function through in vitro and in vivo models. This study emphasizes the notable influence of PFO toxins on intestinal barrier integrity in the context of C. perfringens infections. It reveals that PFO toxins increase ROS production by causing mitochondrial damage, triggering Pyroptosis in IPEC-J2 cells, and consequently resulting in compromised intestinal barrier function. These results offer a scientific foundation for developing preventive and therapeutic approaches against C. perfringens infections.

Keywords

C. perfringens type C; Clostridium perfringens Theta toxin; IPEC-J2; intestinal barrier; pyroptosis.

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