The role of the globular heads of the C1q receptor in TcdA-induced human colonic epithelial cell apoptosis via a mitochondria-dependent pathway

Clostridioides (formerly Clostridium) difficile infection is the leading cause of antibiotic-associated colitis. Studies have demonstrated that C. difficile toxin A (TcdA) can cause apoptosis of many human cell types. The purpose of this study was to investigate the relationships among exposure to T...

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Published in:BMC microbiology 2020-09, Vol.20 (1), p.274-274, Article 274
Main Authors: Liang, Jinhua, Ning, Yongzhong, Dong, Li, Ma, Xiufeng, Li, Shu, Yang, Heran, Li, Qi, Chen, Ling, Gao, Lingjuan, Xu, Yanmin
Format: Article
Language:English
Subjects:
Antibiotics
Apoptosis
ATP
Cell viability
Cells (Biology)
Clostridium difficile
Colitis
DNA nucleotidylexotransferase
Epithelial cells
Flow cytometry
gC1qR
Gene expression
Health aspects
Immunohistochemistry
Infection
Membrane potential
Mitochondria
Mitochondrial function, apoptosis
Morphology
Polymerase chain reaction
Protein expression
Proteins
Reactive oxygen species
Receptors
TcdA
Tetrazolium salt
Toxin A
Toxins
Western blotting
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Summary:Clostridioides (formerly Clostridium) difficile infection is the leading cause of antibiotic-associated colitis. Studies have demonstrated that C. difficile toxin A (TcdA) can cause apoptosis of many human cell types. The purpose of this study was to investigate the relationships among exposure to TcdA, the role of the receptor for the globular heads of C1q (gC1qR) gene and the underlying intracellular apoptotic mechanism in human colonic epithelial cells (NCM 460). In this study, gC1qR expression was examined using real-time polymerase chain reaction (PCR), western blotting and immunohistochemical staining. Cell viability was assessed by the water-soluble tetrazolium salt (WST-1) assay, and cell apoptosis was assessed by flow cytometry and the terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling (TUNEL) assay. Mitochondrial function was assessed based on reactive oxygen species (ROS) generation, changes in the mitochondrial membrane potential (ΔΨm) and the content of ATP. Our study demonstrated that increasing the concentration of TcdA from 10 ng/ml to 20 ng/ml inhibited cell viability and induced cell apoptosis (p 
ISSN:1471-2180
1471-2180
DOI:10.1186/s12866-020-01958-6