Gene expression based evidence of innate immune response activation in the epithelium with oral lichen planus

• Published in: Archives of oral biology 2014-03, Vol.59 (3), p.354-361
• Main Authors: Adami, Guy R, Yeung, Alexander C.F, Stucki, Grant, Kolokythas, Antonia, Sroussi, Herve Y, Cabay, Robert J, Kuzin, Igor, Schwartz, Joel L
• Format: Article
• Language: English
• Subjects: Adolescent; Adult; Advanced Basic Science; Aged; Case-Control Studies; Chemokine CXCL1 - genetics; Dentistry; Epithelial Cells - cytology; Epithelium; Female; Gene Expression; Humans; Immunoenzyme Techniques; Innate immunity; Interleukin-8 - genetics; Lichen planus; Lichen Planus, Oral - genetics; Lichen Planus, Oral - immunology; Lipopolysaccharide Receptors - genetics; Male; Middle Aged; Reverse Transcriptase Polymerase Chain Reaction; RNA; Toll-Like Receptor 1 - genetics
• ISSN: 0003-9969; 1879-1506
• DOI: 10.1016/j.archoralbio.2013.12.010

Abstract Objective Oral lichen planus (OLP) is a disease of the oral mucosa of unknown cause producing lesions with an intense band-like inflammatory infiltrate of T cells to the subepithelium and keratinocyte cell death. We performed gene expression analysis of the oral epithelium of lesions in subjects with OLP and its sister disease, oral lichenoid reaction (OLR), in order to better understand the role of the keratinocytes in these diseases. Design Fourteen patients with OLP or OLR were included in the study, along with a control group of 23 subjects with a variety of oral diseases and a normal group of 17 subjects with no clinically visible mucosal abnormalities. Various proteins have been associated with OLP, based on detection of secreted proteins or changes in RNA levels in tissue samples consisting of epithelium, stroma, and immune cells. The mRNA level of twelve of these genes expressed in the epithelium was tested in the three groups. Results Four genes showed increased expression in the epithelium of OLP patients: CD14, CXCL1, IL8, and TLR1, and at least two of these proteins, TLR1 and CXCL1, were expressed at substantial levels in oral keratinocytes. Conclusions Because of the large accumulation of T cells in lesions of OLP it has long been thought to be an adaptive immunity malfunction. We provide evidence that there is increased expression of innate immune genes in the epithelium with this illness, suggesting a role for this process in the disease and a possible target for treatment.