AB0131 RESPIRATORY TRACT POLY(I:C) STIMULATION ACCELERATES SALIVARY GLAND IMMUNE DYSFUNCTION IN SPONTANEOUS SJOGREN’S SYNDROME ANIMAL MODEL
Authors: P. Hu, B. Ming, X. Wu, L. Dong
Journal: Annals of the Rheumatic Diseases (2020)

Background: Sjogren’s syndrome is one of the most common autoimmune diseases, with a prevalence of 0.33% to 0.77% in Chinese people, characterized by focal infiltration of lymphocytes in glands and the production of multiple autoantibodies. Studies have shown that virus infection may play a crucial role in the occurrence and development of this disease. Objectives: It has been shown that airway stimulation with poly(I:C) can mimic respiratory tract viral infection to some extent. Thus, this study was aimed to investigate the dynamic immune responses in salivary gland after respiratory tract poly(I:C) stimulation in NOD mice. Methods: The 5-week-old NOD mice were given respiratory tract poly(I:C) stimulation to mimic the respiratory virus infection once every other day for a total of 5 times (the total dose is 100μg), and the control group were given the same dose of sterile PBS. After 8 weeks, the mice were sacrificed to obtain and analyze the salivary gland tissues. Results: We found that the salivary gland flow rate was decreased and the blood glucose was influenced by the Viroid stimulation during the early stage in poly(I:C) stimulated group compared with that in PBS group. Accordingly, the pathological injury of salivary gland tissues in poly(I:C) stimulated group was more serious, including decreased volumes of the salivary glands, increased number of pathological focus score and the increased area of lymphocyte infiltration. Furthermore, we found that the expression of IL-33 in salivary glands of poly(I:C) stimulated NOD mice was increased, especially the expression of IL-33 in the acini and ducts. Moreover, the expression of IFN-I and IFN-II is up-regulated in salivary glands. Conclusion: The results of this study suggest that respiratory tract poly(I:C) stimulation accelerates salivary gland immune dysfunction in spontaneous sjogren’s syndrome NOD mice, which mechanisms need to be further investigated. References: [1] Pathogenetic mechanisms in the initiation and perpetuation of Sjogren’s syndrome. Nat Rev Rheumatol 2010; 6: 529-537. [2]Primary Sjögren’s Syndrome. N Engl J Med.2018 378(10):931-939. [3]Epidemiology of primary Sjögren’s syndrome: a systematic review and meta-analysis. Ann Rheum Dis 2015; 74: 1983-9. [4]Vitamin D insufficiency in a large MCTD population. Autoimmun Rev 10:317–324. [5]Epstein-Barr virus persistence and infection of autoreactive plasma cells in synovial lymphoid structures in rheumatoid arthritis. Ann Rheum Dis 72:1559–1568 [6]Liew, F., Girard, J. &amp; Turnquist, H. Interleukin-33 in health and disease. Nat Rev Immunol 16, 676–689 (2016) doi:10.1038/nri.2016.95 [7]Interleukin-33 and the function of innate lymphoid cells. Trends in Immunology, August 2012, Vol. 33, No. 8 [8]Increased Levels of Interleukin 33 in Sera and Synovial Fluid from Patients with Active Rheumatoid Arthritis YASUSHI MATSUYAMA et al The Journal of Rheumatology January 2010, 37 (1) 18-25 [9]Potential involvement of the IL-33-ST2 axis in the pathogenesis of primary Sjogren’s syndrome, Ann Rheum Dis, 2014, 73(6): 1259-1263. [10]The Interleukin 33/ST2 axis in patients with primary Sjogren syndrome: expression in serum and salivary glands, and the clinical association, J Rheumatol, 2015, 42(2): 264-271. [11]Kok MR, Baum BJ, Tak PP, et al Use of localised gene transfer to develop new treatment strategies for the salivary component of Sjögren’s syndrome Annals of the Rheumatic Diseases 2003;62:1038-1046. Acknowledgments: NO Disclosure of Interests: None declared