Loading…

Immune-expression of HSP27 and IL-10 in recurrent aphthous ulceration

Background:  Recently, abnormal cellular immune response has been considered responsible for the oral lesion in the recurrent aphthous ulceration (RAU). For reasons not yet defined, antigens of the oral microbiota would trigger abnormal Th1 immune response against epithelial cells. On the other hand...

Full description

Saved in:
Bibliographic Details
Published in:Journal of oral pathology & medicine 2008-09, Vol.37 (8), p.462-467
Main Authors: Miyamoto Jr, Nelson T., Borra, Ricardo Carneiro, Abreu, Marilda, Weckx, Luc Louis Maurice, Franco, Marcello
Format: Article
Language:English
Subjects:
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Background:  Recently, abnormal cellular immune response has been considered responsible for the oral lesion in the recurrent aphthous ulceration (RAU). For reasons not yet defined, antigens of the oral microbiota would trigger abnormal Th1 immune response against epithelial cells. On the other hand, studies have demonstrated that heat shock proteins (HSP) can block the production of proinflammatory cytokine through inhibition of NF‐κB and mitogen‐activated protein kinase pathways or activate anti‐inflammatory cytokines and therefore control the magnitude of the immune response. HSP27 has been considered a powerful inductor of IL‐10, a major inhibitor of Th1 response. Methods:  Using immunohistochemistry, we studied the expression and location of HSP27 and IL‐10 in ulcerated lesions clinically diagnosed as RAU (n = 27) and to compare it with that of oral clinically normal mucosa (CT; n = 6) and of other inflammatory chronic diseases such as oral fibrous inflammatory hyperplasia (FIH; n = 18), Crohn’s disease (CD; n = 10) and ulcerative colitis (UC; n = 9). Results:  A lower proportion of HSP27‐positive epithelial cells in RAU and CD were observed when compared with CT and FIH (P 
ISSN:0904-2512
1600-0714
DOI:10.1111/j.1600-0714.2008.00665.x