Cargando…
Altered composition of the oral microbiome in integrin beta 6-deficient mouse
In periodontal disease (PD), bacterial biofilms suppress β6 integrin expression transforming growth factor-β1 signaling, resulting in gingival inflammation and bone loss. β6 integrin-null (Itgb6(−/−)) mice develop spontaneous PD. The aim of this study was to unravel potential differences in oral mic...
Autores principales: | , , , , , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Taylor & Francis
2022
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9481083/ https://www.ncbi.nlm.nih.gov/pubmed/36117552 http://dx.doi.org/10.1080/20002297.2022.2122283 |
Sumario: | In periodontal disease (PD), bacterial biofilms suppress β6 integrin expression transforming growth factor-β1 signaling, resulting in gingival inflammation and bone loss. β6 integrin-null (Itgb6(−/−)) mice develop spontaneous PD. The aim of this study was to unravel potential differences in oral microbiome in wild-type (WT) and Itgb6(−/−) FVB mice. Mouse oral microbiome was analyzed from 3- and 6-month-old WT and Itgb6(−/−). The periodontal inflammation and spontaneous bone loss were present in 3-month-old and advanced in 6-month-old Itgb6(−/−) mice. The observed amplicon sequence variants (ASVs) of alpha diversity showed close similarity in 3-month-old and 6-month-old Itgb6(−/−) mice. Chao1 and ACE methods revealed that the microbiome in Itgb6(−/−) mice showed less diversity compared to the WT. UniFrac Principal Coordinate analyses (PCoA) showed a clear spatial segregation and clustering between Itgb6(−/−) and WT mice in general, and between 3-month- and 6-month-old WT mice. Weighted PCoA showed the tight clustering and distinct separation of individual mouse samples within Itgb6(−/−) and WT. The most abundant microbial classes varied between the sample groups. However, the genus Aggregatibacter significantly increased in the 6-month-old Itgb6(−/−) mice. β6 integrin-deficient mice develop periodontal inflammation that may relate to dysbiosis in the microbiome that further promotes the disease process. |
---|