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

NPJ Biofilms Microbiomes. 2020 Oct 30;6(1):49. doi: 10.1038/s41522-020-00158-4.

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adaptor Proteins, Signal Transducing / deficiency*
  • Animals
  • Bacteria / classification*
  • Bacteria / genetics
  • Bacteria / isolation & purification
  • DNA, Bacterial / genetics
  • DNA, Ribosomal / genetics
  • Dysbiosis / etiology*
  • Dysbiosis / microbiology
  • Female
  • Gene Knockout Techniques
  • Mice
  • Mouth / microbiology*
  • Phenotype
  • RNA, Ribosomal, 16S
  • Sialadenitis / genetics
  • Sialadenitis / microbiology*

Substances

  • Adaptor Proteins, Signal Transducing
  • DNA, Bacterial
  • DNA, Ribosomal
  • Nfkbiz protein, mouse
  • RNA, Ribosomal, 16S