Chronic hyperplastic candidiasis (CHC) is characterized by epithelial hyperplasia of the oral mucosa associated with candidal hyphae. The immune status of host is one of the factors that induce clinically evident candidal infection. Host defense mechanisms include inflammatory cells, epithelial barrier, and antimicrobial peptides such as human beta 2 defensin (hBD-2). In the present study, we investigated the densities of CD4+/CD8+ T lymphocytes and hBD-2 expression of epithelial cells in CHC. Immunohistochemical staining was performed on 10 cases of CHC using CD4, CD8 and hBD-2. Ten specimens of chronic mucositis were selected for comparison, and went through the same examination. hBD-2 was expressed in the spinous cell layers and the keratin layers of 7 CHC patients, while the epithelium of chronic mucositis did not demonstrate the hBD-2 expression except for one case. Also, hBD-2 expression was stronger when the hyphae invaded the upper stratum spinosum (P =.019). However, the densities of CD8+ T lymphocytes were significantly lower in the CHC patients, suggesting that the ability of CD8+ T cells to enter the epithelium and target the pathogenic hyphae was decreased in CHC. Increased hBD-2 expression seemed to be significantly associated with the candidal infection, while not promoting the cell-mediated immune reaction in CHC.

Human β- defensin-2 (hBD-2) is an antimicrobial peptide which is produced by epithelial cells after stimulation with microorganisms or inflammatory mediators. However, little is known as to whether the LPS and nicotine induces the expression of hBD-2 in periodontal l igament (PDL) cells. T he p urpose o f this s tudy was t o investigate t he r oles o f MAPKs pathway o f nicotine a nd L PS-induced hBD-2 expression in PDL cells. The maximal expression of hBD-2 was observed in nicotine 5 mM and LPS 1 μg/ml treated PDL cells. Nicotine and LPS induced the phosphorylation of p38, c-Jun N-terminal kinase 1 and 2 (JNK1/2), and extracellular signal-regulated kinases 1 and 2 (ERK1/2) MAPK. ERK1/2 inhibitor SB203580, p38 inhibitor PD98059, and JNK inhibitor SP600125, blocked the effects of nicotine and LPS on hBD-2 upregulation in PDL cells. These results collectively suggest that hBD-2 is up-regulated in nicotine and LPS-treated PDL cells through activation of p38, ERK and JNK MAPKs pathway. Our data regarding the up-regulation of hBD-2 may help us to understand the antimicrobial mechanism in periodontal disease