기관회원 [로그인]
소속기관에서 받은 아이디, 비밀번호를 입력해 주세요.
개인회원 [로그인]

비회원 구매시 입력하신 핸드폰번호를 입력해 주세요.
본인 인증 후 구매내역을 확인하실 수 있습니다.

회원가입
서지반출
Treponema denticola Suppresses Expression of Human ${eta}$-Defensin-2 in Gingival Epithelial Cells through Inhibition of TNF${alpha}$ Production and TLR2 Activation
[STEP1]서지반출 형식 선택
파일형식
@
서지도구
SNS
기타
[STEP2]서지반출 정보 선택
  • 제목
  • URL
돌아가기
확인
취소
  • Treponema denticola Suppresses Expression of Human ${eta}$-Defensin-2 in Gingival Epithelial Cells through Inhibition of TNF${alpha}$ Production and TLR2 Activation
  • Treponema denticola Suppresses Expression of Human ${eta}$-Defensin-2 in Gingival Epithelial Cells through Inhibition of TNF${alpha}$ Production and TLR2 Activation
저자명
Shin. Ji-Eun,Choi. Young-Nim
간행물명
Molecules and cells
권/호정보
2010년|29권 4호|pp.407-412 (6 pages)
발행정보
한국분자세포생물학회
파일정보
정기간행물|ENG|
PDF텍스트
주제분야
기타
이 논문은 한국과학기술정보연구원과 논문 연계를 통해 무료로 제공되는 원문입니다.
서지반출

기타언어초록

We previously reported that Treponema denticola, a periodontal pathogen, suppressed the expression of human ${eta}$-defensins (HBDs) and IL-8 in human gingival epithelial cells. To clarify the receptor(s) involved in the suppression of HBD-2, immortalized gingival epithelial (HOK-16B) cells were infected with live or heat-killed T. denticola for 24 h, and the expression of HBD-2 was examined by real-time RT-PCR. Live T. denticola, but not heat-killed bacteria, suppressed the expression of HBD-2 about 40%. Time courses of suppression revealed that T. denticola suppressed HBD-2 expression only at late time points, which was accompanied with the suppression of TNF${alpha}$ production. Neutralization of TNF${alpha}$ with an antibody abrogated the suppressive effect of T. denticola on HBD-2. Accordingly, heat-killed T. denticola did not suppress TNF${alpha}$ production. Knock-down of toll-like receptor (TLR) 2 via RNA interference reversed the suppressive effect of T. denticola on the expression of HBD-3, but not on the production of TNF${alpha}$. Collectively, T. denticola suppresses the expression of HBD-2 in gingival epithelial cells by inhibiting the TLR2 axis and TNF${alpha}$ production, which may contribute to the pathogenesis of periodontitis by T. denticola.