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Injury of Macrophages Induced by Clostridium perfringens Type C Exotoxins
Siyu Zhang1, Dong Wang1, Yawen Ding1
1Key Laboratory of Ministry of Education for Conservation and Utilization of Special Biological Re-Sources in the Western China, College of Life Science, Ningxia University, Yinchuan 750021, China.
Abstract:
Clostridium perfringens is a kind of anaerobic Gram-positive bacterium that widely exists in the intestinal tissue of humans and animals. And the main virulence factor in Clostridium perfringens is its exotoxins. Clostridium perfringens type C is the main strain of livestock disease, its exotoxins can induce necrotizing enteritis and enterotoxemia, which lead to the reduction in feed conversion, and a serious impact on breeding production performance. Our study found that treatment with exotoxins reduced cell viability and triggered intracellular reactive oxygen species (ROS) in human mononuclear leukemia cells (THP-1) cells. Through transcriptome sequencing analysis, we found that the levels of related proteins such as heme oxygenase 1 (HO-1) and ferroptosis signaling pathway increased significantly after treatment with exotoxins. To investigate whether ferroptosis occurred after exotoxin treatment in macrophages, we confirmed that the protein expression levels of antioxidant factors glutathione peroxidase 4/ferroptosis-suppressor-protein 1/the cystine/glutamate antiporter solute carrier family 7 member 11 (GPX4/FSP1/xCT), ferroptosis-related protein nuclear receptor coactivator 4/transferrin/transferrin receptor (NCOA4/TF/TFR)/ferritin and the level of lipid peroxidation were significantly changed. Based on the above results, our study suggested that Clostridium perfringens type C exotoxins can induce macrophage injury through oxidative stress and ferroptosis.
Insights
Clostridium perfringens type C exotoxins harm livestock by causing intestinal disease. These toxins induce oxidative stress and ferroptosis in macrophages, damaging cells and impacting animal health.
Area of Science:
- Microbiology
- Immunology
- Toxicology
Background:
- Clostridium perfringens type C is a significant livestock pathogen.
- Bacterial exotoxins are key virulence factors contributing to disease.
- Necrotizing enteritis and enterotoxemia reduce livestock productivity.
Purpose of the Study:
- To investigate the cellular mechanisms by which Clostridium perfringens type C exotoxins induce damage.
- To determine the role of oxidative stress and ferroptosis in exotoxin-mediated cellular injury.
Main Methods:
- Treatment of human mononuclear leukemia (THP-1) cells with C. perfringens type C exotoxins.
- Assessment of cell viability and reactive oxygen species (ROS) production.
- Transcriptome sequencing to analyze protein expression changes.
- Confirmation of ferroptosis markers and lipid peroxidation levels in macrophages.
Main Results:
- Exotoxin treatment reduced THP-1 cell viability and increased ROS.
- Transcriptome analysis revealed increased heme oxygenase 1 (HO-1) and ferroptosis pathway proteins.
- Significant alterations in antioxidant factors (GPX4/FSP1/xCT), ferroptosis regulators (NCOA4/TF/TFR/ferritin), and lipid peroxidation were observed.
- Evidence suggests ferroptosis induction following exotoxin exposure.
Conclusions:
- Clostridium perfringens type C exotoxins induce macrophage injury.
- Oxidative stress and ferroptosis are key mechanisms underlying this exotoxin-induced cellular damage.
- Understanding these pathways can inform strategies to mitigate livestock disease caused by C. perfringens type C.
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