WZW is the corresponding author. All authors read and approved the final manuscript. The authors declare that they have no competing interests. “
“Although periodontal tissue is continually challenged by microbial plaque, it is generally maintained in a healthy state. To understand the basis for this, we

investigated innate antiviral immunity in human periodontal tissue. The expression of mRNA encoding different antiviral proteins, myxovirus resistance A (MxA), protein kinase R (PKR), oligoadenylate synthetase GDC-0449 in vivo (OAS), and secretory leukocyte protease inhibitor (SLPI) were detected in both healthy tissue and that with periodontitis. Immunostaining data consistently showed higher MxA protein expression in the epithelial layer of healthy gingiva as compared with tissue with periodontitis. Human MxA is thought to be induced by type I and III interferons (IFNs) but neither cytokine type was detected in healthy periodontal tissues. Treatment in vitro of primary human gingival epithelial cells (HGECs) with α-defensins, but not with the antimicrobial peptides β-defensins or LL-37, led to MxA protein expression. α-defensin was also detected in healthy periodontal tissue. In addition, MxA in α-defensin-treated HGECs was associated with protection against avian influenza H5N1 infection and silencing of the MxA gene using MxA-targeted-siRNA abolished this antiviral activity. To our knowledge, this is the first study to uncover

a novel pathway of human MxA Rebamipide induction, which is initiated by an endogenous antimicrobial peptide, namely α-defensin. This pathway may play an important role in the first line of antiviral selleckchem defense in periodontal tissue. Periodontal tissue is a tooth-supporting structure, which includes gingiva, periodontal ligaments, cementum, and alveolar bone. Chronic inflammation of the periodontal tissue, periodontal disease, is one of the most common inflammatory diseases in humans. The advanced form of the disease, periodontitis, with severe bone destruction may cause tooth loss. The etiologic importance

of bacteria in periodontal disease has been well recognized. Bacterial plaque biofilms continually form on the tooth surfaces adjacent to gingiva. Recent studies have proposed that viral co-infection could enhance the development and progression of periodontitis [[1, 2]]. Detection of herpes simplex virus (HSV) types 1 and 2, human cytomegalovirus (CMV), Epstein-Barr virus (EBV), and human immunodeficiency virus (HIV), have been reported in dental plaque biofilm, gingival crevicular fluid, and periodontitis tissue specimens [[3]]. In healthy periodontal specimens, some viral deoxyribonucleic acid (DNA) can also be found, but generally at lower levels than in periodontitis [[4-6]]. Even so, the precise role of viruses in periodontal disease remains unclear. Periodontal tissue is continually exposed to bacterial plaque; therefore an effective innate immune response is critical to maintain homeostasis.