Association of a dysbiotic oral microbiota with the development of focal lymphocytic sialadenitis in IκB-ζ-deficient mice

• Published in: NPJ biofilms and microbiomes Vol. 6; no. 1; p. 49
• Main Authors: Lee, Junho, Alam, Jehan, Choi, Eunji, Ko, Yeon Kyeong, Lee, Ahreum, Choi, Youngnim
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 30.10.2020; Nature Publishing Group
• Subjects: 631/326/2565/2134; 692/698/2741/2135; 692/700/3032; Biomedical and Life Sciences; Environmental factors; Genotype & phenotype; Life Sciences; Medical Microbiology; Microbial Ecology; Microbial Genetics and Genomics; Microbiology; Microbiota; Microorganisms; Phenotypes; Salivary gland; Sjogren's syndrome; Weaning
• ISSN: 2055-5008; 2055-5008
• DOI: 10.1038/s41522-020-00158-4

Mice lacking IκB-ζ, a protein encoded by the Nfkbiz gene, spontaneously develop a Sjögren’s syndrome-like disease involving the lachrymal glands, but no salivary gland symptoms have been reported. We found that Nfkbiz −/− female mice presented a significantly reduced salivary flow rate, focal lymphocytic sialadenitis (FLS), and a dysbiotic oral microbiota at week 24. To dissect the contributions of genetic and environmental factors to the salivary gland phenotype, Nfkbiz +/+ and Nfkbiz −/− mice were cohoused after weaning and evaluated at week 20. Cohousing alleviated the salivary gland phenotype of Nfkbiz −/− mice but did not induce any disease phenotype in Nfkbiz +/+ mice. Additionally, the oral microbiota in the cohoused mice was synchronized toward that in Nfkbiz +/+ mice. In conclusion, IκB-ζ-deficient mice developed hyposalivation and FLS, in which a dysbiotic oral microbiota played an important role. This finding suggests that the dysbiotic oral microbiota could be a therapeutic target.