Altered composition of the oral microbiome in integrin beta 6-deficient mouse

Abstract

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.

Keywords: 16S ribosomal RNA; QIIME 2; oral microbiome; Β6 integrin-null mouse.