Cathepsin‐cleaved Bid promotes apoptosis in human neutrophils via oxidative stress‐induced lysosomal membrane permeabilization

@article{Blomgran2007CathepsincleavedBP,
  title={Cathepsin‐cleaved Bid promotes apoptosis in human neutrophils via oxidative stress‐induced lysosomal membrane permeabilization},
  author={Robert Blomgran and Limin Zheng and Olle Stendahl},
  journal={Journal of Leukocyte Biology},
  year={2007},
  volume={81}
}
Lysosomal membrane permeabilization (LMP) is emerging as an important regulator of cell apoptosis. Human neutrophils are highly granulated phagocytes, which respond to pathogens by exhibiting increased production of reative oxygen species (ROS) and lysosomal degranulation. In a previous study, we observed that intracellular, nonphagosomal generation of ROS triggered by adherent bacteria induced ROS‐dependent neutrophil apoptosis, whereas intraphagosomal production of ROS during phagocytosis had… 
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Induction of apoptosis in human neutrophils by Mycobacterium tuberculosis is dependent on mature bacterial lipoproteins.

Subversion of a Lysosomal Pathway Regulating Neutrophil Apoptosis by a Major Bacterial Toxin, Pyocyanin1

This study investigated the mechanisms of pyocyanin-induced neutrophil apoptosis and described the first description of a bacterial toxin using a lysosomal cell death pathway, which may be a pathological pathway of cell death to which neutrophils are particularly susceptible, and could be therapeutically targeted to limit neutrophIL death and preserve host responses.

TNF&agr;-induced lysosomal membrane permeability is downstream of MOMP and triggered by caspase-mediated NDUFS1 cleavage and ROS formation

The novel finding that LMP induced by the addition of TNF&agr; plus cycloheximide (CHX), the release of lysosomal cathepsins and ROS formation do not occur upstream but downstream of MOMP and require the caspase-3-mediated cleavage of the p75 NDUFS1 subunit of respiratory complex I is presented.

Lysosomal membrane permeabilization in cell death

The regulation of LMP is perturbed in cancer cells, suggesting that specific strategies for LMP induction might lead to novel therapeutic avenues.

A Cardinal Role for Cathepsin D in Co-Ordinating the Host-Mediated Apoptosis of Macrophages and Killing of Pneumococci

It is shown that lysosomal membrane permeabilization (LMP) and cytosolic translocation of activated cathepsin D occur prior to activation of a mitochondrial pathway of macrophage apoptosis in pulmonary host defense and underscores the importance of apoptosis-associated microbial killing to macrophages function.

Cysteine Cathepsins Trigger Caspase-dependent Cell Death through Cleavage of Bid and Antiapoptotic Bcl-2 Homologues*

It is proposed that degradation of anti-apoptotic Bcl-2 family members by lysosomal cathepsins synergizes with cathepsypsin-mediated activation of Bid to trigger a mitochondrial pathway to apoptosis.

Regulation of apoptosis-associated lysosomal membrane permeabilization

A growing body of evidence suggests that LMP may be governed by several distinct mechanisms that are likely engaged in a death stimulus- and cell-type-dependent fashion, and factors contributing to permeabilization of the lysosomal membrane including reactive oxygen species, lysOSomal membrane lipid composition, proteases, p53, and Bcl-2 family proteins are described.

Anthrax Lethal Toxin Induced Lysosomal Membrane Permeabilization and Cytosolic Cathepsin Release Is Nlrp1b/Nalp1b-Dependent

A role for lysosomal membrane permeabilization in the cellular response to bacterial pathogens is revealed and a shared requirement for cytosolic relocalization of cathepsins in pyroptosis and pyronecrosis is demonstrated.

Mycobacterium tuberculosis-induced apoptotic neutrophils trigger a pro-inflammatory response in macrophages through release of heat shock protein 72, acting in synergy with the bacteria.

Constitutive neutrophil apoptosis: Mechanisms and regulation

The current understanding regarding the modulation of neutrophil apoptotic death by various extracellular stimuli such as proinflammatory cytokines, cell adhesion, phagocytosis, red blood cells, and platelets is summarized.
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