Association of a dysbiotic oral microbiota with the development of focal lymphocytic sialadenitis in IκB-ζ-deficient mice
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 lympho...
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| Published in | NPJ biofilms and microbiomes Vol. 6; no. 1; p. 49 |
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| Main Authors | , , , , , |
| Format | Journal Article |
| Language | English |
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30.10.2020
Nature Publishing Group |
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| Abstract | 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. |
|---|---|
| AbstractList | 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. 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. Abstract 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. |
| ArticleNumber | 49 |
| Author | Lee, Junho Lee, Ahreum Choi, Eunji Choi, Youngnim Alam, Jehan Ko, Yeon Kyeong |
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| Snippet | 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... Abstract Mice lacking IκB-ζ, a protein encoded by the Nfkbiz gene, spontaneously develop a Sjögren’s syndrome-like disease involving the lachrymal glands, but... 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... |
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| Title | Association of a dysbiotic oral microbiota with the development of focal lymphocytic sialadenitis in IκB-ζ-deficient mice |
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