Funda Erbasan1, Arsenal Sezgin Alikanoğlu2, Veli Yazısız3, Uğur Karasu1, Ayşe Balkarlı1, Cem Sezer2, Mustafa Ender Terzioğlu4. 1. Department of Rheumatology, Antalya Training and Research Hospital, Antalya, Turkey. 2. Department of Pathology, Antalya Training and Research Hospital, Antalya, Turkey. 3. Department of Internal Medicine, Division Of Rheumatology, Antalya, Turkey. Electronic address: drvyazisiz@yahoo.com.tr. 4. Department of Internal Medicine, Division Of Rheumatology, Antalya, Turkey.
Abstract
BACKGROUND: The role of leptin in primary Sjögren's syndrome (SS) pathogenesis is unknown. The aim of this study was to investigate the expression of leptin and leptin receptor (LEPR) in minor salivary glands in patients with SS. MATERIALS AND METHODS: The expression of leptin and LEPR in minor salivary gland specimens obtained from patients with primary SS (n=50) and control subjects (n=50) were examined using immunohistochemical staining. RESULTS: Acinar cells, epithelial cells and adipocytes in salivary glands can express leptin and LEPR. It was observed that there was intense staining in the focal lymphocytic infiltration areas in SS patients. The intensity of leptin and LEPR staining under microscopy (400×) were graded semiquantitatively as negative, mild, moderate or strongly positive, and scored as 1, 2 or 3, respectively. The expression levels of leptin and LEPR in patients with primary SS were not higher than in controls. There was no significant difference in degrees of leptin and LEPR staining, staining intensity, and immunoreactive scores between groups. The expression of leptin and LEPR were not correlated with autoantibodies such as RF, ANA, anti-Ro, and/or anti-La positivity. CONCLUSIONS: These findings indicate that leptin and its receptors do not play an important role in primary SS pathophysiology.
BACKGROUND: The role of leptin in primary Sjögren's syndrome (SS) pathogenesis is unknown. The aim of this study was to investigate the expression of leptin and leptin receptor (LEPR) in minor salivary glands in patients with SS. MATERIALS AND METHODS: The expression of leptin and LEPR in minor salivary gland specimens obtained from patients with primary SS (n=50) and control subjects (n=50) were examined using immunohistochemical staining. RESULTS: Acinar cells, epithelial cells and adipocytes in salivary glands can express leptin and LEPR. It was observed that there was intense staining in the focal lymphocytic infiltration areas in SS patients. The intensity of leptin and LEPR staining under microscopy (400×) were graded semiquantitatively as negative, mild, moderate or strongly positive, and scored as 1, 2 or 3, respectively. The expression levels of leptin and LEPR in patients with primary SS were not higher than in controls. There was no significant difference in degrees of leptin and LEPR staining, staining intensity, and immunoreactive scores between groups. The expression of leptin and LEPR were not correlated with autoantibodies such as RF, ANA, anti-Ro, and/or anti-La positivity. CONCLUSIONS: These findings indicate that leptin and its receptors do not play an important role in primary SS pathophysiology.