Localization of antimicrobial peptides human β-defensins in minor salivary glands with Sjögren's syndrome

• Published in: European journal of oral sciences 2009-10, Vol.117 (5), p.506-510
• Main Authors: Kaneda, Yoshihiro, Yamaai, Tomoichiro, Mizukawa, Nobuyoshi, Nagatsuka, Hitoshi, Yamachika, Eiki, Gunduz, Mehmet, Sawaki, Koichi, Yamanishi, Yuji, Matsubara, Masakazu, Katase, Naoki, Takagi, Shin
• Format: Article
• Language: English
• Subjects: Arthritis, Rheumatoid - complications; beta-Defensins - analysis; defensin; Dentistry; Disease Progression; Epithelial Cells - pathology; Female; Humans; Immunohistochemistry; Male; Middle Aged; minor salivary gland; Saliva - metabolism; Salivary Ducts - pathology; Salivary Glands, Minor - metabolism; Salivary Glands, Minor - pathology; Secretory Rate - physiology; Sjogren's Syndrome - classification; Sjogren's Syndrome - pathology; Sjogren's Syndrome - physiopathology; Sjögren's syndrome
• ISSN: 0909-8836; 1600-0722
• DOI: 10.1111/j.1600-0722.2009.00667.x

Sjögren’s syndrome is a common systemic autoimmune disease associated with inflammatory cells that infiltrate exocrine glands. The antimicrobial peptides human β‐defensin‐1, human β‐defensin‐2, and human β‐defensin‐3 are expressed in various human epithelial cells and in normal salivary glands. Antimicrobial peptides provide local protection against infection and participate in inflammatory responses. Because of the presence of inflammation, we hypothesized that human β‐defensin expression in minor salivary glands may be increased in subjects with Sjögren’s syndrome. However, the expression of human β‐defensins 1 and 2 was decreased in salivary glands affected by Sjögren’s syndrome in comparison with the human β‐defensin expression patterns in salivary glands from normal subjects. In addition, the reduction in expression of human β‐defensin‐2 was greater than the reduction in expression of human β‐defensin‐1. The aforementioned result suggests that the reduction in expression of human β‐defensin‐2 may occur earlier than the reduction in expression of human β‐defensin‐1, which may lead to a greater decrease in human β‐defensin‐2 than in human β‐defensin‐1 during disease progression.