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

Citation
K. Amin et al., Inflammation and structural changes in the airways of patients with primary Sjogren's syndrome, RESP MED, 95(11), 2001, pp. 904-910
Citations number
26
Categorie Soggetti
Cardiovascular & Respiratory Systems","da verificare
Journal title
RESPIRATORY MEDICINE
ISSN journal
09546111 → ACNP
Volume
95
Issue
11
Year of publication
2001
Pages
904 - 910
Database
ISI
SICI code
0954-6111(200111)95:11<904:IASCIT>2.0.ZU;2-E
Abstract
The present study aimed to compare the cellular pattern and structural chan ges in the airways of patients with primary Sjogren's syndrome (pSS) with h ealthy controls. Bronchial biopsy specimens were obtained from seven subjec ts with pSS and seven healthy controls. All the patients with pSS had incre ased bronchial responsiveness to methacholine. In the biopsies inflammatory cells, cytokine-producing cells, tenascin and laminin were visualized by i mmunostaining. Patients with pSS had a higher number of neutrophils and mas t 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 but the numbers of IL-4-and IL-5-positive cells were not significantly differen t 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-positi ve cells were similar to the healthy controls. The degree of epithelial int egrity in patients with pSS was significantly lower than in the control gro up and the tenascin and laminin layers were significantly thicker in the pS S group. There was a correlation between the number of mast cells and the t hickness of the tenascin and laminin layers in pSS. In conclusion, we found that the cellular pattern in the bronchial mucosa of patients with pSS dis played large numbers of neutrophils, mast cells and T-lymphocytes. These ch anges in inflammatory cell numbers seemed to relate to the observed increas ed epithelial damage and structural changes of the subepithelium. The struc tural findings, but not the pattern of inflammatory cells, are shared with atopic asthma and may relate to the increased bronchial hyper-responsivenes s seen in both diseases. (C) 2001 Harcourt Publishers Ltd.