Abstract
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.
Key Indexing Terms:Footnotes
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E.A. Boström, DDS; H. Forsblad d’Elia, MD, PhD; U. Dahlgren, DDS, PhD, Professor, Department of Rheumatology and Inflammation Research; C. Simark-Mattsson, DDS, PhD, Department of Endodontology/Oral Diagnosis; B. Hasséus, DDS, PhD, Section of Oral Immunology, Clinic for Oral Medicine; H. Carlsten, MD, PhD, Professor; A. Tarkowski, MD, PhD, Professor; M. Bokarewa, MD, PhD, Associate Professor, Department of Rheumatology and Inflammation Research.
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Supported by grants from the Medical Society of Gothenburg, the Swedish Association against Rheumatism, the King Gustaf V Foundation, the Swedish Medical Research Council, the Inflammation Network, the Nanna Svartz Foundation, AME Wolff Foundation, Rune and Ulla Amlövs Trust, Swedish Foundation for Strategic Research, and the University of Gothenburg.
- Accepted for publication May 28, 2008.
