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Aphthous stomatitis - computational biology suggests external biotic stimulus and immunogenic cell death involved
Ignacio Riveros-Gomez1, Joaquin Vasquez-Marin1, Elisa Ximena Huerta-Garcia1
1Laboratorio de Histopatología Oral y Maxilofacial, Unidad de Medicina Oral y Patología Oral, Departamento de Estomatología, Facultad de Odontología, Universidad de Talca, Avenida Lircay S/N, Campus Norte Universidad de Talca, Edificio de Ciencias Biomédicas, Oficina N°4, Talca, 3460000, Región del Maule, Chile.
Background:
The exact cause of recurrent aphthous stomatitis is still unknown, making it a challenge to develop effective treatments. This study employs computational biology to investigate the molecular basis of recurrent aphthous stomatitis, aiming to identify the nature of the stimuli triggering these ulcers and the type of cell death involved.
Methods:
To understand the molecular underpinnings of recurrent aphthous stomatitis, we used the Génie tool for gene identification, targeting those associated with cell death in recurrent aphthous stomatitis. The ToppGene Suite was employed for functional enrichment analysis. We also used Reactome and InteractiVenn for protein integration and prioritization against a PANoptosis gene list, enabling the construction of a protein-protein interaction network to pinpoint key proteins in recurrent aphthous stomatitis pathogenesis.
Results:
The study's computational approach identified 1,375 protein-coding genes linked to recurrent aphthous stomatitis. Critical among these were proteins responsive to bacterial stimuli, especially high mobility group protein B1 (HMGB1), toll-like receptor 2 (TLR2), and toll-like receptor 4 (TLR4). The enrichment analysis suggested an external biotic factor, likely bacterial, as a triggering agent in recurrent aphthous stomatitis. The protein interaction network highlighted the roles of tumor necrosis factor (TNF), NF-kappa-B essential modulator (IKBKG), and tumor necrosis factor receptor superfamily member 1A (TNFRSF1A), indicating an immunogenic cell death mechanism, potentially PANoptosis, in recurrent aphthous stomatitis.
Conclusion:
The findings propose that bacterial stimuli could trigger recurrent aphthous stomatitis through a PANoptosis-related cell death pathway. This new understanding of recurrent aphthous stomatitis pathogenesis underscores the significance of oral microbiota in the condition. Future experimental validation and therapeutic strategy development based on these findings are necessary.
Insights
Recurrent aphthous stomatitis may be triggered by bacterial stimuli activating a PANoptosis cell death pathway. This computational study identifies key genes and proteins involved in the condition
Area of Science:
- Computational biology
- Molecular biology
- Immunology
Background:
- The exact cause of recurrent aphthous stomatitis (RAS) remains unknown, hindering effective treatment development.
- Computational biology approaches are utilized to explore the molecular basis of RAS.
- Identifying triggers and cell death mechanisms in RAS is crucial for therapeutic advancement.
Purpose of the Study:
- To investigate the molecular underpinnings of recurrent aphthous stomatitis using computational biology.
- To identify stimuli that trigger RAS ulcers and the specific cell death pathways involved.
- To construct a protein-protein interaction network for key protein identification in RAS pathogenesis.
Main Methods:
- Gene identification using the Génie tool, focusing on cell death-associated genes in RAS.
- Functional enrichment analysis performed with ToppGene Suite.
- Protein integration and prioritization using Reactome and InteractiVenn against a PANoptosis gene list.
Main Results:
- Identification of 1,375 protein-coding genes associated with RAS.
- Key proteins responsive to bacterial stimuli include HMGB1, TLR2, and TLR4.
- Protein interaction network implicated TNF, IKBKG, and TNFRSF1A, suggesting PANoptosis as a potential cell death mechanism.
Conclusions:
- Bacterial stimuli may trigger RAS via a PANoptosis-related cell death pathway.
- Oral microbiota plays a significant role in the pathogenesis of RAS.
- Further experimental validation and therapeutic strategies targeting these pathways are warranted.
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