Experimental Murine Periodontitis Increases Salivary Gland IgA-Producing B Cells Following Oral Dysbiosis
doi: 10.1111/1348-0421.13191.
Online ahead of print.
Affiliations
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Microbiol Immunol.
.
Abstract
The oral microbiome is closely involved in the maintenance of host health and the development of systemic diseases. The salivary glands play an essential role in homeostasis in the oral cavity. Here, we investigated the effects of periodontal inflammation on salivary gland function and the oral microbiome. In experimental periodontitis model mice, an increase in IgA⁺ cells in the salivary glands were observed 1 week after treatment. Alteration of the oral microbiome was also induced in this model. Gene expression analysis of the salivary glands showed changes in the expression of genes related to B-cell maturation and plasma cell differentiation and an increase in the expression of genes related to macrophage activation upon experimental periodontitis induction. Furthermore, the relationship between disruption of oral microflora and salivary gland function was examined using a cohousing model in which experimental periodontitis model mice and untreated mice were reared in the same cage. We found that cohoused normal mice underwent alteration of the oral microbiome, with increases in IgA⁺ cells and macrophages in the salivary glands. In summary, our results suggest that, in the oral cavity, there is a close link between oral bacterial flora and immune cells in the salivary glands. Our results also show that localized inflammation disrupts the homeostasis in the oral cavity, inducing pathological conditions such as dysbiosis. Our study suggests the importance of the interaction among local oral inflammation, salivary gland function, and oral microflora, and provides new insights into the mechanisms by which oral health is maintained.
Keywords:
IgA; dysbiosis; mucosal immunology; oral microbiome; periodontal inflammation; salivary gland.
© 2024 The Author(s). Microbiology and Immunology published by The Societies and John Wiley & Sons Australia, Ltd.
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Fonte original PubMed