Increased beta 2 defensin in recurrent aphthous ulcer.

Abstract

OBJECTIVES:

It was hypothesized that beta 2 defensin (BD-2) is increased in RAU lesions compared with healthy controls to promote anti-microbial host defence.

METHODS:

RAU and control mucosa samples were subjected to quantitative real-time PCR and immunostained for BD-2, CD68, mast cell tryptase and 4-hydroxynonenal (4HNE). The effect of tumour necrosis factor-α (TNF-α) ± interleukin-17C (IL-17C), without and with vitamin K3, was studied on BD-2 expression in epithelial SCC-25 cells.

RESULTS:

Although BD-2 mRNA did not differ between healthy and RAU mucosa, BD-2 stained strongly in acute-phase RAU epithelium (P = 0.001). In controls, subepithelial BD-2(+) cells were mast cells and macrophages, whereas in RAU, most infiltrating leucocytes were BD-2(+) (P = 0.004). In cell culture, BD-2 was increased 124-fold by TNF-α (P < 0.0001) and 208-fold synergistically together with IL-17C (P < 0.0001). 4HNE staining of RAU epithelium was not significantly increased, and vitamin K3-induced reactive oxygen species (ROS) did not affect BD-2.

CONCLUSIONS:

Anti-microbial BD-2 was not affected by oxidative stress but was highly increased in the epithelial and immigrant cells in the acute-phase RAU lesions, probably in part synergistically by TNF-α and epithelial IL-17C, which are known to be induced by activation of danger-signal receptors by pathogen- and/or damage-associated molecular patterns.

• Authors: A Al-Samadi, A Salem, M Ainola, J Hietanen, R Häyrinen-Immonen, Y T Konttinen
• Journal: Oral diseases (Oral Dis) Vol. 21 Issue 3 Pg. 292-8 (Apr 2015) ISSN: 1601-0825 [Electronic] Denmark
• PMID: 24854020 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
• Copyright: © 2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.

Chemical References

• Aldehydes
• DEFB4A protein, human
• Interleukin-17
• RNA, Messenger
• Tumor Necrosis Factor-alpha
• beta-Defensins
• 4-hydroxy-2-nonenal

Topics

• Adult
• Aldehydes (metabolism)
• Case-Control Studies
• Cell Line
• Female
• Gene Expression
• Humans
• Interleukin-17 (metabolism)
• Male
• Middle Aged
• Mouth Mucosa (metabolism, pathology)
• Oxidative Stress
• RNA, Messenger (metabolism)
• Stomatitis, Aphthous (genetics, metabolism, pathology)
• Tumor Necrosis Factor-alpha (pharmacology)
• Young Adult
• beta-Defensins (genetics, metabolism)