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Modulation of Antimicrobial Peptide Human β-defensin-3 by Toll-like Receptor Ligands in Vaginal Epithelial Cells
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Seo Yeon Lee, Hae jong Kim, In Ho Chang, June Hyun Han, Kyung Do Kim, Young Tae Moon, Soon Chul Myung
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Korean J Urogenit Tract Infect Inflamm 2014;9(1):27-33. Published online April 30, 2014
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 Abstract
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- Purpose
Vaginal epithelial cells have always been exposed to various pathogens. However, this has not always caused clinical infection. In addition to a previously reported protection effect of the vagina, currently, the innate immune response is thought to be important as one of the causes explaining the phenomenon. Therefore, we investigated the innate immunity of the vagina and related mechanisms in infected vaginal epithelial cells focusing on the antimicrobial peptide human β-defensin-3 (HBD-3).
Materials and Methods: We investigated the signaling molecules, Toll-like receptors (TLRs), through which mammals sense infection in vaginal epithelial cells, with activation with lipopolysaccharide (LPS), Staphylococcus aureus peptidoglycan (PGN), or zymosan. Reverse transcriptase-polymerase chain reaction analysis of HBD-3 messenger RNA expression in vaginal epithelial cells after treatment with three pathogens was performed for investigation of pathogen-associated molecular patterns. Then, we also studied the following mechanism of innate immunity of the vagina focusing on HBD-3 in vaginal epithelial cells infected with gram-positive bacteria, gram-negative bacteria, or fungus.
Results: Vaginal epithelial cells (VK2/E6E7 cells) constitutively expressed TLR2 and TLR4 and produced antimicrobial peptide HBD-3 upon activation with LPS, PGN, or zymosan. VK2/E6/E7 cells exposed to LPS, PGN, or zymosan showed increased p38 mitogen activated protein kinase (MAPK) activity. In addition, LPS-, PGN-, and zymosan-induced HBD-3 expression was attenuated by SB203580, a p38 MAPK inhibitor, emphasizing the importance of p38 MAPK in induction of HBD-3.
Conclusions: Vaginal epithelial cells may contribute to the host innate immune defense upon exposure to gram-negative bacteria, gram-positive bacteria, or fungi in the vagina by upregulation of HBD-3 expression.
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