지원사업
학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
커뮤니티
연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2012.9
- 수록면
- 201 - 209 (9page)
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초록· 키워드
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Apoptosis is a physiological programmed cell death process. Tubercle bacilli inhibit apoptosis of alveolar macrophages and phagolysosome fusion. We investigated whether the Bcl-2 family anti-apoptotic member, Bfl-1/A1, plays an important role in the anti-apoptotic process during mycobacterial infection. PMA-treated human monocytoid THP-1 cells were infected with mycobacteria (H37Rv, BCG, and K-strain) at a multiplicity of infection (MOI) of 10 for 0, 1.5, 3, 6, 9, 12, 18, 24, 48, or 72 h. In addition, PMA-treated THP-1 cells were pretreated with specific inhibitors for 45 min before stimulation with mycobacteria at an MOI of 10 for 4 h. After the indicated time, the cells were subject to reverse transcription-polymerase chain reaction (RT-PCR) analysis, and a Bfl-1/A1-specific Western blot was performed. In PMA-differentiated THP-1 cells, the expression level of Bfl-1/A1 mRNA was increased by Mycobacterium tuberculosis (MTB) H37Rv infection. The mRNA level of Bfl-1/A1 peaked 3 h after MTB infection, then declined gradually until 9 h. However, Bfl-1/A1 mRNA induction gradually re-increased from 24 h to 72 h after MTB infection. No difference in Bfl-1/A1 expression was detected following infection with MTB H37Rv, K-strain, or M. bovis BCG. These results were not dependent on mycobacterial virulence. Moreover, mRNA levels of other anti-apoptotic molecules (Mcl-1, Bcl-2, and Bcl-xL) were not increased after MTB H37Rv or K-strain infection. These results suggest that mycobacteria induce the innate immune host defense mechanisms that utilize Bfl-1/A1 molecules at early time points, regardless of virulence.
목차
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
참고문헌 (31)
참고문헌 신청
Armstrong JA / 1971 / Response of cultured macrophages to Mycobacterium tuberculosis, with observations on fusion of lysosomes with phagosomes / J Exp Med 134:713~740
Bocchino M / 2005 / Role of mycobacteria-induced monocyte/macrophage apoptosis in the pathogenesis of human tuberculosis / Int J Tuberc Lung Dis 9:375~383
Chan J / 1992 / Killing of virulent Mycobacterium tuberculosis by reactive nitrogen intermediates produced by activated murine macrophages / J Exp Med 175:1111~1122
Clemens DL / 1995 / Characterization of the Mycobacterium tuberculosis phagosome and evidence that phagosomal maturation is inhibited / J Exp Med 181:257~270
Deretic V / 2006 / Mycobacterium tuberculosis inhibition of phagolysosome biogenesis and autophagy as a host defence mechanism / Cell Microbiol 8:719~727
Bocchino M / 2005 / Role of mycobacteria-induced monocyte/macrophage apoptosis in the pathogenesis of human tuberculosis / Int J Tuberc Lung Dis 9:375~383
Chan J / 1992 / Killing of virulent Mycobacterium tuberculosis by reactive nitrogen intermediates produced by activated murine macrophages / J Exp Med 175:1111~1122
Clemens DL / 1995 / Characterization of the Mycobacterium tuberculosis phagosome and evidence that phagosomal maturation is inhibited / J Exp Med 181:257~270
Deretic V / 2006 / Mycobacterium tuberculosis inhibition of phagolysosome biogenesis and autophagy as a host defence mechanism / Cell Microbiol 8:719~727
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UCI(KEPA) : I410-ECN-0101-2014-510-001368801