Journal
NPJ BIOFILMS AND MICROBIOMES
Volume 6, Issue 1, Pages -Publisher
NATURE RESEARCH
DOI: 10.1038/s41522-020-00158-4
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Funding
- National Research Foundation of Korea [2018R1A5A2024418, 2020R1A2C2007038]
- National Research Foundation of Korea [2018R1A5A2024418, 2020R1A2C2007038] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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Mice lacking I kappa B-zeta, a protein encoded by the Nfkbiz gene, spontaneously develop a Sjogren'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, I kappa B-zeta-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.
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