S-R Nandula1, Y M Scindia, P Dey, H Bagavant, U S Deshmukh. 1. Division of Nephrology, Center for Immunity Inflammation and Regenerative Medicine, University of Virginia, Charlottesville, VA 22908, USA.
Abstract
OBJECTIVE: Sjögren's syndrome is a chronic autoimmune disorder characterized by progressive lymphocytic infiltration within the salivary and lacrimal glands. This study was undertaken to investigate the effects of innate immunity activation on sialoadenitis in a mouse strain genetically susceptible for development of SS-like disease. METHODS: Female New Zealand Black X New Zealand White F1 mice were repeatedly treated with toll-like 3 receptor agonist poly(I:C). Submandibular glands were investigated at different time points for sialoadenitis by immunohistochemistry and for gene expression of different chemokines by quantitative PCR. Submandibular gland-infiltrating cells were characterized by flow cytometry. RESULTS: Poly(I:C) treatment significantly upregulated the expression of multiple chemokines within the submandibular glands. The severity and incidence of sialoadenitis was considerably higher in poly(I:C)-treated mice. There was a preponderance of dendritic cells and NK cells in the initial inflammatory cell infiltrates, and these were followed by CD4+ T cells. CONCLUSIONS: Our data clearly demonstrate that systemic activation of innate immunity accelerates sialoadenitis in a mouse model for SS-like disease. These findings suggest that chronic activation of innate immunity can influence certain features of SS.
OBJECTIVE: Sjögren's syndrome is a chronic autoimmune disorder characterized by progressive lymphocytic infiltration within the salivary and lacrimal glands. This study was undertaken to investigate the effects of innate immunity activation on sialoadenitis in a mouse strain genetically susceptible for development of SS-like disease. METHODS: Female New Zealand Black X New Zealand White F1 mice were repeatedly treated with toll-like 3 receptor agonist poly(I:C). Submandibular glands were investigated at different time points for sialoadenitis by immunohistochemistry and for gene expression of different chemokines by quantitative PCR. Submandibular gland-infiltrating cells were characterized by flow cytometry. RESULTS:Poly(I:C) treatment significantly upregulated the expression of multiple chemokines within the submandibular glands. The severity and incidence of sialoadenitis was considerably higher in poly(I:C)-treated mice. There was a preponderance of dendritic cells and NK cells in the initial inflammatory cell infiltrates, and these were followed by CD4+ T cells. CONCLUSIONS: Our data clearly demonstrate that systemic activation of innate immunity accelerates sialoadenitis in a mouse model for SS-like disease. These findings suggest that chronic activation of innate immunity can influence certain features of SS.
Authors: Hiroaki Moriyama; Li Wen; Norio Abiru; Edwin Liu; Liping Yu; Dongmei Miao; Roberto Gianani; F Susan Wong; George S Eisenbarth Journal: Proc Natl Acad Sci U S A Date: 2002-04-09 Impact factor: 11.205
Authors: Barbara M Szczerba; Paulina Kaplonek; Nina Wolska; Anna Podsiadlowska; Paulina D Rybakowska; Paromita Dey; Astrid Rasmussen; Kiely Grundahl; Kimberly S Hefner; Donald U Stone; Stephen Young; David M Lewis; Lida Radfar; R Hal Scofield; Kathy L Sivils; Harini Bagavant; Umesh S Deshmukh Journal: Ann Rheum Dis Date: 2015-02-05 Impact factor: 19.103
Authors: Virginia A Carroll; Alyssa Lundgren; Hairong Wei; Susan Sainz; Kenneth S Tung; Michael G Brown Journal: J Virol Date: 2011-12-07 Impact factor: 5.103
Authors: N C Kyriakidis; E K Kapsogeorgou; V C Gourzi; O D Konsta; G E Baltatzis; A G Tzioufas Journal: Clin Exp Immunol Date: 2014-12 Impact factor: 4.330
Authors: B M Szczerba; P D Rybakowska; P Dey; K M Payerhin; A B Peck; H Bagavant; U S Deshmukh Journal: J Dent Res Date: 2013-03-26 Impact factor: 6.116