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conferenceseries.com
May 01-02, 2017 Toronto, Canada
2nd International Conference on
Restorative Dentistry and Prosthodontics
Volume 5, Issue 1 (Suppl) J Oral Hyg Health
ISSN: 2332-0702 JOHH, an open access journal Restorative Dentistry & Prosthodontics 2017
May 01-02, 2017
Wang Wenmei, J Oral Hyg Health 2017, 5:1 (Suppl)
Cigarette smoke regulates the expression of human β defensins via NOD1/RIP2 signal pathway in human
oral mucosa
Wang Wenmei
Nanjing University, China
Smoking is a well recognized risk for periodontitis, oral candidiasis, oral leukoplakia and oral cancer. Cigarette smoke has been
confirmed to dampen innate immune in some human tissues, such as oral mucosa. The epithelium of oral mucosa acts as a
defense shield against microorganisms and other harmful stimulating factors such as smoking. Nucleotide binding oligomerization
domain 1 (NOD1) signal pathway and human β defensins (hBDs) play crucial roles in innate immune. So far there is very little
study about the effect of smoking on local innate immune response of oral mucosa. Therefore, the aim of this study was to evaluate
potential effects of smoking on NOD1 signaling expression in oral mucosa. Tissue specimens of normal oral mucosa were collected
from donors undergoing routine surgical treatment. All 20 participants were classified equally as two groups: Non-smokers and
smokers. By using Western blotting and immunohistochemistry, we investigated differential expression of NOD1 and RIP2, using
immunohistochemistry to detect hBD-1, -2, and -3 in oral mucosa tissues between non-smokers and smokers. Immortalized human
oral mucosal epithelial (Leuk-1) cells were treated with various concentrations of cigarette smoke extract (CSE) for 24 h. Western
blotting and immunofluorescence assays were performed to study CSE-induced alteration of NOD1 and RIP2 protein expression.
The change of hBDs expression were tested using immunofluorescence, qPCR, and ELISA. Leuk-1 cells were treated with 4% CSE, iE-
DAP (NOD1 agonist), CSE + iE-DAP. And then Real-time PCR and ELISA were performed to detect the mRNA levels and secretion
of hBD-1, -2, and -3, respectively. The results showed that the levels of NOD1, hBD-1 and hBD-3 were significantly reduced in oral
mucosa tissues of smokers compared with non-smokers. The levels of RIP2 and hBD-2 were remarkably enhanced in oral mucosa
tissues of smokers. CSE treatment suppressed NOD1 expression and activated RIP2 expression in Leuk-1 cells. The mRNA and
secretory levels of hBD-1 and -3 were down-regulated by CSE, while the mRNA and secretory level of hBD-2 were up-regulated by
CSE. The iE-DAP treatment reversed the regulatory effects of CSE. The present study indicated that cigarette smoke could potentially
modulate the expression of crucial molecules of NOD1 signal pathway and hBDs in human oral mucosal epithelium. NOD1 signal
pathway played an important role in the regulatory effects of CSE on hBDs levels in oral mucosal epithelial cells.
Biography
Wang Wenmei is a Professor, and Deputy-Dean of Nanjing Stomatological Hospital, Medical School of Nanjing University, a well-known specialized subject hospital
in China. In recent years, she has participated in more than 9 research projects, presided over 2 National Natural Scientific Funding of China. She has published
more than 100 papers, of which 16 were included by SCI. She has been serving as an Editorial Board Member of the Clinics in Oncology, Journal of Dentistry and
Oral Biology, SM Journal of Public Health & Epidemiology, International Journal of Oral and Craniofacial Science, SM Dentistry Journal, etc. And she has been
serving as a Reviewer of the Neurotoxicity Research, Journal of Cellular Physiology, and Cancer Research Frontiers. She has won a number of honors and awards,
including “Scientific and Technological Progress Award” of Jiangsu Province, “Medical Scientific and Technological Award of Jiangsu Province”, “Scientific and
Technological Progress Award” of Nanjing City, “New Technological introduction Award” from the Health Department of Jiangsu Province, etc.