Role of Cathepsin S in Periodontal Inflammation and Infection

• Main Authors: S. Memmert, A. Damanaki, A. V. B. Nogueira, S. Eick, M. Nokhbehsaim, A. K. Papadopoulou, A. Till, B. Rath, S. Jepsen, W. Götz, C. Piperi, E. K. Basdra, J. A. Cirelli, A. Jäger, J. Deschner
• Format: Article
• Language: English
• Published: Hindawi Limited 2017-01-01
• Series: Mediators of Inflammation
• Online Access: http://dx.doi.org/10.1155/2017/4786170
• ISSN: 0962-9351; 1466-1861

Cathepsin S is a cysteine protease and regulator of autophagy with possible involvement in periodontitis. The objective of this study was to investigate whether cathepsin S is involved in the pathogenesis of periodontal diseases. Human periodontal fibroblasts were cultured under inflammatory and infectious conditions elicited by interleukin-1β and Fusobacterium nucleatum, respectively. An array-based approach was used to analyze differential expression of autophagy-associated genes. Cathepsin S was upregulated most strongly and thus further studied in vitro at gene and protein levels. In vivo, gingival tissue biopsies from rats with ligature-induced periodontitis and from periodontitis patients were also analyzed at transcriptional and protein levels. Multiple gene expression changes due to interleukin-1β and F. nucleatum were observed in vitro. Both stimulants caused a significant cathepsin S upregulation. A significantly elevated cathepsin S expression in gingival biopsies from rats with experimental periodontitis was found in vivo, as compared to that from control. Gingival biopsies from periodontitis patients showed a significantly higher cathepsin S expression than those from healthy gingiva. Our findings provide original evidence that cathepsin S is increased in periodontal cells and tissues under inflammatory and infectious conditions, suggesting a critical role of this autophagy-associated molecule in the pathogenesis of periodontitis.