Apoptosis is an innate defense function of macrophages against Mycobacterium tuberculosis

S. M. Behar, C. J. Martin, M. G. Booty, T. Nishimura, X. Zhao, H. X. Gan, M. Divangahi, H. G. Remold

研究成果: Review article査読

254 被引用数 (Scopus)

抄録

Two different forms of death are commonly observed when Mycobacterium tuberculosis (Mtb)-infected macrophages die: (i) necrosis, a death modality defined by cell lysis and (ii) apoptosis, a form of death that maintains an intact plasma membrane. Necrosis is a mechanism used by bacteria to exit the macrophage, evade host defenses, and spread. In contrast, apoptosis of infected macrophages is associated with diminished pathogen viability. Apoptosis occurs when tumor necrosis factor activates the extrinsic death domain pathway, leading to caspase-8 activation. In addition, mitochondrial outer membrane permeabilization leading to activation of the intrinsic apoptotic pathway is required. Both pathways lead to caspase-3 activation, which results in apoptosis. We have recently demonstrated that during mycobacterial infection, cell death is regulated by the eicosanoids, prostaglandin E 2 (proapoptotic) and lipoxin (LX)A 4 (pronecrotic). Although PGE 2 protects against necrosis, virulent Mtb induces LXA 4 and inhibits PGE 2 production. Under such conditions, mitochondrial inner membrane damage leads to macrophage necrosis. Thus, virulent Mtb subverts eicosanoid regulation of cell death to foil innate defense mechanisms of the macrophage.

本文言語English
ページ(範囲)279-287
ページ数9
ジャーナルMucosal Immunology
4
3
DOI
出版ステータスPublished - 2011 5月
外部発表はい

ASJC Scopus subject areas

  • 免疫アレルギー学
  • 免疫学

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