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.
摘要:
产气荚膜梭菌(C.产气荚膜),革兰氏阳性细菌,产生各种毒素和胞外酶,可导致人类和动物的疾病。常见症状包括腹部肿胀,腹泻,和肠道炎症。严重的病例会导致肠出血等并发症,水肿,甚至死亡。导致产气荚膜梭菌感染肠道发病的主要毒素是CPA,CPB,CPB2、CPE、和PFO。其中,CPB,CPB2和CPE参与细胞凋亡的发展,虽然注册会计师与细胞死亡有关,细胞内ROS水平增加,炎症因子IL-18的释放。然而,PFO毒素在受感染的肠道中发挥作用的确切机制尚不清楚。该研究表明,产气荚膜梭菌PFO毒素感染通过体外和体内模型破坏肠上皮屏障功能。这项研究强调了在产气荚膜梭菌感染的背景下,PFO毒素对肠屏障完整性的显着影响。它揭示了PFO毒素通过引起线粒体损伤来增加ROS的产生,触发IPEC-J2细胞的焦亡,从而导致肠屏障功能受损。这些结果为开发针对产气荚膜梭菌感染的预防和治疗方法提供了科学依据。