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- Original Article Modulation of Antimicrobial Peptide Human β-defensin-3 by Toll-like Receptor Ligands in Vaginal Epithelial Cells
- 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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질상피세포에서 Toll-like Receptor Ligands에 의한 항생 펩티드 Human β-defensin-3의 발현조절 - 이소연, 김해종, 장인호, 한준현, 김경도, 문영태, 명순철
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Urogenital Tract Infection 2014;9(1):27-33.
Published online: April 30, 2014
Department of Urology, Myongji Hospital, Goyang,
1Functional Food Research Center, School of Life Sciences and Biotechnology, Korea University,
2Department of Urology, Chung-Ang University College of Medicine, Seoul,
3Department of Urology, Hallym University Dongtan Sacred Heart Hospital, Hallym University College of Medicine, Hwaseong,
4Advanced Urogenital Disease Research Center, Chung-Ang University Hospital, Seoul, Korea
명지병원 비뇨기과,
1고려대학교 생명과학대학 건강기능식품연구센터,
2중앙대학교 의과대학 비뇨기과학교실,
3한림대학교 의과대학 한림대학교
1Functional Food Research Center, School of Life Sciences and Biotechnology, Korea University,
2Department of Urology, Chung-Ang University College of Medicine, Seoul,
3Department of Urology, Hallym University Dongtan Sacred Heart Hospital, Hallym University College of Medicine, Hwaseong,
4Advanced Urogenital Disease Research Center, Chung-Ang University Hospital, Seoul, Korea
명지병원 비뇨기과,
1고려대학교 생명과학대학 건강기능식품연구센터,
2중앙대학교 의과대학 비뇨기과학교실,
3한림대학교 의과대학 한림대학교
Received: 11 January 2014 • Revised: 29 January 2014 • Accepted: 3 February 2014
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Abstract
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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