Dying to live: how the death modality of the infected macrophage affects immunity to tuberculosis.
Dying to live: how the death modality of the infected macrophage affects immunity to tuberculosis.
复制标题
死于生命：感染巨噬细胞的死亡方式如何影响对结核病的免疫。
DOI：
10.1007/978-1-4614-6111-1_6
复制
发表时间：
2013
影响因子：
--
通讯作者：
Remold H
中科院分区：
文献类型：
--
作者：
Divangahi M;Behar SM;Remold H
VirulentMycobacterium tuberculosis(Mtb) inhibits apoptosis and triggers necrosis of host macrophages to evade innate delay in the initiation of adaptive immunity. Necrosis is a mechanism used by bacteria to exit macrophage, evade the host defenses, and disseminate while apoptosis is associated with diminished pathogen viability. We have recently demonstrated that eicosanoids regulate cell death program of either human or murine macrophages infected withMtb. We have defined prostaglandin E2(PGE2) as a pro-apoptotic host lipid mediator which protects against necrosis. In contrast, lipoxin A4(LXA4) is a pro-necrotic lipid mediator which suppresses PGE2synthesis, resulting in mitochondrial damage and inhibition of plasma membrane repair mechanisms; this ultimately leads to the induction of necrosis. Thus, the balance between PGE2and LXA4determines whetherMtb-infected macrophages undergo apoptosis or necrosis and this balance determines the outcome of infection.
