Effects of Bacterial Lipopolysaccharide or Lipoteichoic Acid on Infection of Herpes Simplex Virus Type 1 in Oral Cells

• Main Authors: Yu-Jen Pan, 潘譽仁
• Other Authors: Shan-Ling Hung
• Format: Others
• Language: zh-TW
• Published: 2017
• Online Access: http://ndltd.ncl.edu.tw/handle/90366819157614662978

碩士 === 國立陽明大學 === 口腔生物研究所 === 105 === Herpes simplex virus type 1 (HSV-1) is a ubiquitous and highly contagious virus that can cause many human diseases. The common oral diseases are like herpetic gingivostomatitis and herpes labialis. Another common oral disease is periodontal disease. Periodontal disease is a highly prevalent chronic inflammatory disease characterized by destruction of the tissue and bone that support the teeth. It is caused by oral Gram-positive bacteria and Gram-negative bacteria. Recent studies have found that co-infection with HSV and periodontal pathogens is observed in periodontal destructive sites. The purpose of this study is to investigate the effects of bacterial lipopolysaccharide (LPS) or lipoteichoic acid (LTA) on infection of HSV-1 in oral cells. The viral yield was determined by plaque assay. The viral DNA entry, replication and mRNA of cell receptors were determined by quantitative real-time polymerase chain reaction (q-PCR). The entry of viral capsid was determined by immunofluorescence staining analysis. The expression of viral proteins was determined by Western blotting analysis. The release of cytokines was determined by the enzyme-linked immunosorbent assay. The results showed that viral yields were decreased in immortalized normal oral keratinocytes (NOK), which were treated with Pg-LPS or Sa-LTA during HSV-1 infection, but were increased in oral buccal mucosal fibroblast (OF). Furthermore, the results showed that expression of cell receptors and entry of viral capsid were decreased in NOK treated with Pg-LTA or Sa-LTA, but viral DNA replication and expression of viral protein ICP0, ICP5 and glycoprotein D (gD) were not significantly affected. However, the results showed that viral entry, viral DNA replication and viral protein expression were not significantly different in OF treated with Pg-LTA or Sa-LTA compared to the control. The release of interleukin-6 (IL-6) and interleukin-8 (IL-8) was increased in Pg-LPS or Sa-LTA treated OF. The results suggested that viral yield was decreased by Pg-LTA or Sa-LTA in infected NOK, but increased by Pg-LTA or Sa-LTA in infected OF. The key factor responsible for the impact remains to be explored.