Temporal changes in salivary glands of non-obese diabetic mice as a model for Sjögren’s syndrome
Article first published online: 14 SEP 2011
© 2011 John Wiley & Sons A/S
Volume 18, Issue 1, pages 96–106, January 2012
How to Cite
Roescher, N., Lodde, B., Vosters, J., Tak, P., Catalan, M., Illei, G. and Chiorini, J. (2012), Temporal changes in salivary glands of non-obese diabetic mice as a model for Sjögren’s syndrome. Oral Diseases, 18: 96–106. doi: 10.1111/j.1601-0825.2011.01852.x
- Issue published online: 20 DEC 2011
- Article first published online: 14 SEP 2011
- Accepted manuscript online: 16 AUG 2011 09:13AM EST
- Received 1 July 2011; revised 18 July 2011; accepted 3 August 2011
- Sjögren’s syndrome;
- salivary gland;
- autoimmune sialadenitis;
- non-obese diabetic mouse;
Oral Diseases (2011) 18, 96–106
Objective: Non-obese diabetic (NOD) mice develop an autoimmune exocrinopathy that shows similarities with Sjögren’s syndrome. They provide an experimental model to study the pathoetiogenesis of this disease.
Materials and Methods: Salivary gland (SG) function and salivary sodium content were measured in 8-, 12-, 16- and 20-week-old NOD and age-matched CB6 mice. In NOD mice, SG expression of phenotypic cell markers, B cell-stimulating and costimulatory molecules were evaluated. Cytokine levels were measured in serum and SG homogenates.
Results: Microscopically evident SG inflammation in NOD mice was preceded by expression of intercellular adhesion molecule 1 on epithelial cells in the presence of macrophages and relatively high levels of cytokines. Next, an influx consisting of mainly T, B, natural killer, plasma and dendritic cells was seen. Most cytokines, except for interleukin (IL)12/IL23p40 and B cell-activating factor, decreased or remained stable over time, while glandular function deteriorated from 16 weeks of age onward compared with CB6 mice.
Conclusion: Sjögren’s syndrome-like disease in NOD mice occurs in multiple stages; immunological and physiological abnormalities can be detected before focal inflammation appears and salivary output declines. Extrapolating this knowledge to human subjects could help in understanding the pathogenesis and aid the identification of potential therapeutic targets.