Clostridium perfringens (CP) is a foodborne pathogen. The bacterium can also inhabit human gut without symptoms of foodborne illness. However, the clinical symptoms of long-term inhabitation have not been known yet. Therefore, the objective of this study was to elucidate the relationship between intestinal CP and other internal organs. Phosphate-buffered saline (PBS) and CP were orally injected into 5-week-old (YOUNG) and 12-month-old C57BL6/J (ADULT) mice. Gene expression levels related to inflammation (tumor necrosis factor-α [TNF-α], interleukin [IL]-1β, and IL-6) and oxidative stress (superoxide dismutase [SOD]1, SOD2, SOD3, glutathione reductase [GSR], glutathione peroxidase [GPx]3, and catalase [CAT]) responses were evaluated in the brain, small intestine, and liver. In addition, apoptosis-related (BCL2-associated X [BAX]1 and high-mobility group box-1 [HMGB1]) and brain disorder-related genes (CCAAT-enhancer-binding protein [C/EBP]-β, C/EBPδ, C/EBP homologous protein [CHOP], and amyloid precursor protein [APP]) as brain damage markers were examined. The protein expressions in the brain were also measured. Gene expression levels of inflammation and oxidative stress responses were higher (p < 0.05) in brains of CP-YOUNG and CP-ADULT mice, compared with PBS-YOUNG and PBS-ADULT, and the gene expression levels were higher (p < 0.05) in brains of CP-ADULT mice than CP-YOUNG mice. Apoptosis-related (BAX1 and HMGB1) and brain disorder-related genes (C/EBPβ, C/EBPδ, CHOP, and APP) were higher (p < 0.05) in brains of CP-challenged mice, compared with PBS-challenged mice. Even oxidative stress response (GPx and SOD2), cell damage-related (HMGB1), and β-amyloid proteins were higher (p < 0.05) in brains of CP- than in PBS-challenged mice. C/EBP protein was higher (p < 0.05) in CP-YOUNG, compared with PBS-YOUNG mice. However, these clinical symptoms were not observed in small intestine and liver. These results indicate that although asymptomatic intestinal CP do not cause foodborne illness, their inhabitation may cause brain inflammation, oxidative stress, apoptosis, and cell damage, which may induce disorders, especially for the aged group.

中文翻译：

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无症状的产气荚膜梭状芽孢杆菌在肠道中的栖息会导致脑部炎症，细胞凋亡和疾病。

产气荚膜梭状芽胞杆菌（CP）是一种食源性病原体。这种细菌也可以栖息在人类肠道内，而没有食源性疾病的症状。但是，长期居住的临床症状尚不清楚。因此，本研究的目的是阐明肠道CP与其他内部器官之间的关系。将磷酸盐缓冲液（PBS）和CP口服注射到5周龄（YOUNG）和12月龄C57BL6 / J（ADULT）小鼠中。与炎症（肿瘤坏死因子-α[TNF-α]，白介素[IL]-1β和IL-6）和氧化应激（超氧化物歧化酶[SOD] 1，SOD2，SOD3，谷胱甘肽还原酶[GSR]）相关的基因表达水平，谷胱甘肽过氧化物酶[GPx] 3和过氧化氢酶[CAT]）的反应在大脑，小肠和肝脏中进行了评估。此外，凋亡相关基因（BCL2相关X [BAX] 1和高迁移率族box-1 [HMGB1]）和脑部疾病相关基因（CCAAT增强子结合蛋白[C / EBP]-β，C /EBPδ，C检查了/ EBP同源蛋白[CHOP]和淀粉样前体蛋白[APP]作为脑损伤标志物。还测量了大脑中的蛋白质表达。与PBS-YOUNG和PBS-ADULT相比，CP-YOUNG和CP-ADULT小鼠的大脑中炎症和氧化应激反应的基因表达水平更高（p <0.05），并且基因表达水平更高（p <0.05）在CP-ADULT小鼠的脑中比在CP-YOUNG小鼠中高。与受PBS攻击的小鼠相比，受CP攻击的小鼠的大脑中与细胞凋亡相关的基因（BAX1和HMGB1）和与脑部疾病相关的基因（C /EBPβ，C /EBPδ，CHOP和APP）更高（p <0.05）。甚至是氧化应激反应（GPx和SOD2），与CP攻击的小鼠相比，CP-大脑中的细胞损伤相关（HMGB1）和β-淀粉样蛋白更高（p <0.05）。与PBS-YOUNG小鼠相比，CP-YOUNG中的C / EBP蛋白更高（p <0.05）。但是，在小肠和肝脏中未观察到这些临床症状。这些结果表明，尽管无症状的肠道CP不会引起食源性疾病，但它们的栖息可能会引起脑部炎症，氧化应激，细胞凋亡和细胞损伤，从而诱发疾病，尤其是对于老年人群。