Innate Immune Response to Vibrio cholerae β-Barrel Pore-Forming Hemolysin: Unraveling Cytotoxic, Oxidative, and Inflammatory Pathways | ||
| Benha Journal of Applied Sciences | ||
| Volume 10, Issue 2, February 2025, Pages 115-119 PDF (743.08 K) | ||
| Document Type: Original Research Papers | ||
| DOI: 10.21608/bjas.2025.369208.1626 | ||
| Authors | ||
| Ahmed F Abdelrahman1; Dr. Alaa Elmetwalli2; Mohamed. O. Abdel Monem3; Mervat Gameel Hassan* 4 | ||
| 1Bahgat | ||
| 2Sherbin, Mansoura, Egypt | ||
| 3Professor of Botany and Microbiology Department , Faculty of Science, Benha University | ||
| 4Botany and Microbiology Department, Faculty of Science, Benha University, Egypt | ||
| Abstract | ||
| Abstract Background Vibrio cholerae β-barrel pore-forming hemolysin (Vchβ-PFH) is a key virulence factor that disrupts host cell membranes, triggering immune responses. However, the transcriptional landscape of innate immunity in response to Vchβ-PFH remains poorly understood. This study investigates the cytotoxic, oxidative, inflammasome, and immune signaling responses to Vchβ-PFH in macrophage-like THP-1. Methods Cells were exposed to varying concentrations of Vchβ-PFH, and cytotoxicity was assessed using MTT and LDH assays. Oxidative stress levels were quantified via intracellular ROS measurements. Inflammasome activation was evaluated by NLRP3 and IL-1β using qRT-PCR. Immune signaling responses were analyzed by measuring the transcriptional expression of TNF-α, IFN-β, IL-10, and CD200. Primer sequences used for qRT-PCR were designed and validated through Primer-BLAST. Results Exposure to Vchβ-PFH resulted in significant dose-dependent cytotoxicity, as indicated by reduced cell viability and increased LDH release (p < 0.01). ROS levels were markedly elevated, suggesting oxidative stress as a key mechanism of toxin-induced damage. qRT-PCR analysis revealed upregulation of NLRP3, IL-1β, indicating inflammasome activation. Pro-inflammatory cytokines (TNF-α, IFN-β, and IL-1β) were significantly upregulated, while CD200 and IL-10 were also increased, suggesting a potential immune-regulatory feedback mechanism. Conclusion Vchβ-PFH induces cellular cytotoxicity, oxidative stress, inflammasome activation, and immune modulation, revealing its potential role in V. cholerae pathogenesis. These findings highlight novel molecular targets for therapeutic interventions against pore-forming toxin-mediated infections. Further studies are needed to explore the mechanisms underlying host immune evasion and inflammatory resolution in response to V. cholerae hemolysins. | ||
| Keywords | ||
| Vibrio cholerae; β-barrel pore-forming hemolysin; inflammasome activation; oxidative stress; cytokine response | ||
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