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Evaluation of cellular response to Clostridium difficile toxin-A: a network analysis
Babak Arjmand1, Somayeh Jahani Sherafat2, Mostafa Rezaei Tavirani3
1Cell Therapy and Regenerative Medicine Research Center, Endocrinology and Metabolism Molecular-Cellular Sciences Institute, Tehran University of Medical Sciences, Tehran, Iran.
Aim:
The current study aimed to determine crucial genes targeted by toxin-A through network analysis.
Background:
Clostridium difficile (C difficile) produces toxin-A and toxin-B and is known as a risk factor for hospital infection, especially after broad spectrum antibiotic therapy. Bioinformatics findings have led to the introduction of a set of genes and biological terms that are targeted by toxin-B in colon epithelia.
Methods:
The significant differentially expressed genes (DEGs) of human intestinal Caco-2 cells treated by toxin-A versus control were retrieved from gene expression omnibus (GEO). The queried DEGs were analyzed using by protein-protein interaction (PPI) network analysis through STRING database and Cytoscape software v.3.7.2.
Results:
Among 157 significant DEGs, JUN, VEGFA, CDKN1A, ATF3, SNAI1, DUSP1, HSPB1, MCL1, KLF4, FOSL1, HSPA1A, and SQSTM1 were determined as hubs and JUN, DUSP1, DUSP5, EZR, MAP1LC3B, and SQSTM1 were highlighted as bottlenecks.
Conclusion:
JUN, DUSP1, and SQSTM1 are possible drug targets to prevent and treat C difficile infection.
Insights
Network analysis identified key genes targeted by Clostridium difficile toxin-A. JUN, DUSP1, and SQSTM1 emerged as crucial hubs and bottlenecks, representing potential therapeutic targets for C. difficile infections.
Area of Science:
- Molecular biology
- Bioinformatics
- Genomics
Background:
- Clostridium difficile (C. difficile) infection is a significant hospital-acquired risk, often linked to antibiotic use.
- C. difficile produces toxins A and B, which impact colon epithelial cells.
- Previous bioinformatics studies identified genes affected by toxin B.
Purpose of the Study:
- To identify critical genes modulated by C. difficile toxin A using network analysis.
- To explore potential therapeutic targets for C. difficile infections.
Main Methods:
- Differential gene expression analysis of human intestinal Caco-2 cells treated with toxin A.
- Protein-protein interaction (PPI) network analysis using STRING and Cytoscape software.
- Identification of hub and bottleneck genes within the interaction network.
Main Results:
- Analysis of 157 differentially expressed genes (DEGs) revealed key players.
- JUN, VEGFA, CDKN1A, ATF3, SNAI1, DUSP1, HSPB1, MCL1, KLF4, FOSL1, HSPA1A, and SQSTM1 were identified as hub genes.
- JUN, DUSP1, DUSP5, EZR, MAP1LC3B, and SQSTM1 were highlighted as bottleneck genes.
Conclusions:
- JUN, DUSP1, and SQSTM1 are significant targets within the toxin A-mediated cellular network.
- These identified genes represent promising candidates for developing novel therapeutic strategies against C. difficile infections.
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