Inflammation and structural changes in the airways of patients with primary Sjögren's syndrome

Abstract

The present study aimed to compare the cellular pattern and structural changes in the airways of patients with primary Sjögren's syndrome (pSS) with healthy controls. Bronchial biopsy specimens were obtained from seven subjects with pSS and seven healthy controls. All the patients with pSS had increased bronchial responsiveness to methacholine. In the biopsies inflammatory cells, cytokine-producing cells, tenascin and laminin were visual zed by immunostaining. Patients with pSS had a higher number of neutrophils and mast cells than healthy controls, while the number of eosinophils was similar in the two groups. The number of IL-8-positive cells was higher in pSS butthe numbers of IL-4-and IL-5-positive cells were not significantly different between pSS and healthy controls. The numbers of T cells in patients with pSS were higher than in healthy controls, while the numbers of CD25-positive cells were similar to the healthy controls. The degree of epithelial integrity in patients with pSS was significantly lower than in the control group and the tenascin and laminin layers were significantly thicker in the pSS group. There was a correlation between the number of mast cells and the thickness of the tenascin and laminin layers in pSS. In conclusion, we found that the cellular pattern in the bronchial mucosa of patients with pSS displayed large numbers of neutrophils, mast cells and T-lymphocytes. These changes in inflammatory cell numbers seemed to relate to the observed increased epithelial damage and structural changes of the subepithelium. The structural findings, but not the pattern of inflammatory cells, are shared with atopic asthma and may relate to the increased bronchial hyper-responsiveness seen in both diseases.

Tenascin-C Produced by Oxidized LDL-Stimulated Macrophages Increases Foam Cell Formation through Toll-like Receptor-4

“…Previously, studies have shown that increased TN-C levels are observed in multiple autoimmune diseases (Midwood et al, 2009), including rheumatoid arthritis, Sjogren's syndrome (Amin et al, 2001), and diabetes (Loots et al, 1998). Our data shows that exogenous TN-C, together with oxLDL (5 μg/ml) is capable of activating foam cell formation.…”

“…It is not normally expressed in most adult tissues but is specifically and transiently upregulated during acute inflammation and persistently expressed in chronic inflammation (Chiquet-Ehrismann and Chiquet, 2003). Previous studies have shown that increased TN-C levels are observed in multiple autoimmune diseases (Midwood et al, 2009), including rheumatoid arthritis, Sjogren's syndrome (Amin et al, 2001), and diabetes (Loots et al, 1998). However, the potential function of TN-C in foam cell formation and atherosclerosis was barely understood.…”

Small airways diseases, excluding asthma and COPD: an overview

“…10 patients had infiltration of bronchi and bronchiole submucosa by lymphocytes, which were CD4+T-lymphocytes in six patients [56]. Another study described neutrophils and mast cells in the bronchi of patients with primary Sjö gren's syndrome [57]. Finally, a Japanese study found no difference in cells infiltrating small airways between primary and secondary Sjö gren's syndromes [58].…”

Pulmonary Mucosa-associated Lymphoid Tissue (MALT) Lymphoma in Sjögren's Syndrome Showing Only the LIP Pattern Radiologically

“…Furthermore, multifocal cysts were seen in six of 51 patients (two with LIP, two with malignant lymphoma, two with amyloidosis). Some authors have proposed that the formation of bronchioectasis and cystic changes might be due to air-trapping occurring as the result of chronic bronchial inflammation and increased epithelial airway damage by inflammatory cells (20,21). We suggest that some SS patients with multiple cysts in chest CT were complicated with LIP, malignant lymphoma, and amyloidosis (4,18).…”