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Wang, Y., Li, J., & Chen, R. (2024). Emerging concepts in mucosal immunity and oral microecological control of respiratory virus infection-related inflammatory diseases. Microbiological Research, 289, 127930. Added by: Dr. Enrique Feoli (27/12/2025, 12:18) Last edited by: Dr. Enrique Feoli (31/12/2025, 15:35) |
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| Resource type: Journal Article DOI: 10.1016/j.micres.2024.127930 ID no. (ISBN etc.): 0944-5013 BibTeX citation key: Wang2024 View all bibliographic details  |
Categories: ARIA, BioAcyl Corp, BioAcyl Corp Subcategories: Inmunidad de mucosas, Inmunidad de mucosas Keywords: Cytokines storm, IL-17/Th17, Oral microecological, Pulmonary fibrosis, Respiratory viral infections Creators: Chen, Li, Wang Collection: Microbiological Research |
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| Abstract |
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Oral microecological imbalance is closely linked to oral mucosal inflammation and is implicated in the development of both local and systemic diseases, including those caused by viral infections. This review examines the critical role of the interleukin (IL)-17/helper T cell 17 (Th17) axis in regulating immune responses within the oral mucosa, focusing on both its protective and pathogenic roles during inflammation. We specifically highlight how the IL-17/Th17 pathway contributes to dysregulated inflammation in the context of respiratory viral infections. Furthermore, this review explores the potential interactions between respiratory viruses and the oral microbiota, emphasizing how alterations in the oral microbiome and increased production of proinflammatory factors may serve as early, non-invasive biomarkers for predicting the severity of respiratory viral infections. These findings provide insights into novel diagnostic approaches and therapeutic strategies aimed at mitigating respiratory disease severity through monitoring and modulating the oral microbiome.
Added by: Dr. Enrique Feoli Last edited by: Dr. Enrique Feoli |
| Notes |
Oral microecological imbalances and respiratory viral infections produce crude salt cytokines that activate the JAK-STAT signaling pathway, leading to a Treg/Th17 imbalance that promotes an inflammatory response. Important factors in the differentiation of Th17 cells are the activation of signaling sensors and STAT3. Binding of IL-6, IL-21, and IL-23 to the receptor allows JAK to phosphorylate the receptor leading to recruitment and phosphorylation of STAT3. STAT3 then undergoes dimerization and is translocated to the nucleus to enhance the expression of genes. STAT3 induces ROR-γT expression. Th17 cells can produce IL-17 in response to pathogens bodies while inducing pathogenic inflammation. Oral microbiome P. Lipopolysaccharide (LPS) secreted by gingivalis et al. is an important virulence factor, and P. gingivalis-LPS interacts with JAK-STAT signaling pathway through TLR4 receptor, which in turn affects the occurrence and development of inflammation. Added by: Dr. Enrique Feoli Last edited by: Dr. Enrique Feoli |