RT Journal Article
SR Electronic
T1 Salivary Resistin Reflects Local Inflammation in Sjögren’s Syndrome
JF The Journal of Rheumatology
JO J Rheumatol
FD The Journal of Rheumatology
SP 2005
OP 2011
VO 35
IS 10
A1 ELISABETH ALMER BOSTRÖM
A1 HELENA FORSBLAD D’ELIA
A1 ULF DAHLGREN
A1 CHARLOTTE SIMARK-MATTSSON
A1 BENGT HASSÉUS
A1 HANS CARLSTEN
A1 ANDREJ TARKOWSKI
A1 MARIA BOKAREWA
YR 2008
UL http://www.jrheum.org/content/35/10/2005.abstract
AB Objective To assess the role of resistin in primary Sjögren’s syndrome (pSS) and its relation to local inflammation. Methods Blood and saliva were collected from 37 patients with pSS (duration of symptoms 12.6 ± 1 yrs) and 32 healthy controls. Expression of resistin in salivary glands was visualized immunohistologically, and levels of resistin were detected by ELISA. Levels of resistin were evaluated at baseline and following oral dehydroepiandrosterone (DHEA) treatment (50 mg/day). The effect of DHEA treatment on the secretion of resistin was assessed in vitro in human leukocytes after challenge with insulin and lipopolysaccharide. Results Levels of resistin in saliva were significantly higher in patients with pSS than in controls, while circulating levels of resistin were similar in both groups. Resistin was expressed in the epithelial cells of striated ducts and in the lymphocytic foci. Resistin levels in saliva were related to the intensity of inflammation in the minor salivary glands of pSS patients. No changes of the levels of resistin in blood or saliva were observed during DHEA treatment. Exposure of naive leukocytes to DHEA in vitro induced significant expression of resistin compared to nonstimulated peripheral blood mononuclear cells (p = 0.031). Conclusion We showed that levels of resistin are upregulated locally in the salivary glands of patients with pSS; and that the levels of resistin correspond to the intensity of lymphocytic inflammation in patients with pSS. We suggest that resistin is expressed in the salivary glands of patients with pSS and may be a driving factor of local inflammation.