Related Experiment Video

Updated: Jul 11, 2026

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death
09:18

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death

Published on: December 27, 2016

C/EBPbeta phosphorylation rescues macrophage dysfunction and apoptosis induced by anthrax lethal toxin

Martina Buck1, Mario Chojkier

  • 1Department of Medicine, University of California San Diego, and Veterans Affairs Healthcare System, San Diego, CA 92161, USA. mbuck@ucsd.edu

American Journal of Physiology. Cell Physiology
|September 15, 2007
PubMed

Insights

Bacillus anthracis lethal toxin (LT) causes macrophage apoptosis by inhibiting ribosomal S6 kinase-2 (RSK) and CCAAT/enhancer binding protein-beta (C/EBPbeta) activation. Restoring C/EBPbeta function protects against anthrax toxin-induced immune cell death and pathogenesis.

Area of Science:

  • Immunology
  • Molecular Biology
  • Cell Biology

Background:

  • Bacillus anthracis lethal toxin (LT) disrupts immune responses.
  • LT cleaves MAPK kinases, inhibiting antiapoptotic targets, but these targets remain unidentified.

Purpose of the Study:

  • Identify MAPK targets affected by LT.
  • Investigate the role of C/EBPbeta in LT-induced macrophage apoptosis and anthrax pathogenesis.

Main Methods:

  • Assessed macrophage apoptosis and caspase 8 activation.
  • Measured RSK activation and C/EBPbeta phosphorylation.
  • Utilized dominant-positive C/EBPbeta transgenic mice for in vivo studies.

Main Results:

  • LT induced macrophage apoptosis via enhanced caspase 8 activation and suppressed RSK/C/EBPbeta activation.
  • Expression of a phosphorylation mimic C/EBPbeta (C/EBPbeta-E(217)) blocked LT-induced apoptosis.
  • LT impaired macrophage phagocytosis and oxidative burst, which was prevented in C/EBPbeta-E(217) transgenic mice.

Conclusions:

  • C/EBPbeta is a critical target of LT in macrophages.
  • C/EBPbeta plays a significant role in anthrax pathogenesis by regulating macrophage apoptosis and function.

More Related Videos

LPS and ATP-induced Death of PMA-differentiated THP-1 Macrophages and its Validation06:12

LPS and ATP-induced Death of PMA-differentiated THP-1 Macrophages and its Validation

Published on: May 3, 2024

Bone Marrow-derived Macrophage Production07:06

Bone Marrow-derived Macrophage Production

Published on: November 22, 2013

Related Concept Videos

Inhalation Anthrax01:25

Inhalation Anthrax

Anthrax is a zoonotic disease caused by Bacillus anthracis, a Gram-positive, spore-forming bacterium. It primarily affects herbivorous animals but can be transmitted to humans through skin contact, ingestion, or inhalation of spores.Cutaneous anthrax, the most common form, typically results from direct contact with bacterial spores through skin abrasions and is generally less severe. Gastrointestinal anthrax results from eating undercooked or contaminated meat. It affects the mouth, throat, or...
Cellular Injury V: Apoptosis and Autophagy01:22

Cellular Injury V: Apoptosis and Autophagy

Cells respond to damage and stress through highly coordinated processes that decide whether they survive or undergo controlled self-destruction. Two major pathways involved in this regulation are apoptosis, a type of programmed cell death, and autophagy, a survival mechanism that helps cells adapt to adverse conditions.ApoptosisApoptosis removes aged or injured cells to maintain tissue balance. During this process, the cell shrinks, chromatin condenses and fragments, and membrane-bound...
Phagocytosis of Apoptotic Cells01:17

Phagocytosis of Apoptotic Cells

Cells undergoing apoptosis form apoptotic bodies that must be removed immediately to prevent inflammation, autoimmune diseases, and necrosis. Phagocytosis is carried out by professional phagocytes such as macrophages or  immature dendritic cells. Non-professional phagocytes such as  epithelial cells and fibroblasts also take part in this process; however, they are not as effective as professional phagocytes. 
Normal cells contain receptors that prevent them from being recognized by phagocytes.