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KMID : 1234520140090010027
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Korean Journal of Urogenital Tract Infection Inflammation
2014 Volume.9 No. 1 p.27 ~ p.33
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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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Lee Seo-Yeon
Kim Hae-Jong
Chang In-Ho
Han June-Hyun
Kim Kyung-Do
Moon Young-Tae
Myung Soon-Chul
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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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KEYWORD
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Vagina, Beta defensin 3, human, Toll-like receptors
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