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Updated: May 30, 2026

LPS and ATP-induced Death of PMA-differentiated THP-1 Macrophages and its Validation
Published on: May 3, 2024
AMPD3 is involved in anthrax LeTx-induced macrophage cell death
Sangun Lee1, Yanhai Wang, Sung Ouk Kim
1Department of Immunology and Microbial Science, The Scripps Research Institute, La Jolla, CA 92037, USA.
Abstract:
The responses of macrophages to Bacillus anthracis infection are important for the survival of the host, since macrophages are required for the germination of B. anthracis spores in lymph nodes, and macrophage death exacerbates anthrax lethal toxin (LeTx)-induced organ collapse. To elucidate the mechanism of macrophage cell death induced by LeTx, we performed a genetic screen to search for genes associated with LeTx-induced macrophage cell death. RAW264.7 cells, a macrophage-like cell line sensitive to LeTx-induced death, were randomly mutated and LeTx-resistant mutant clones were selected. AMP deaminase 3 (AMPD3), an enzyme that converts AMP to IMP, was identified to be mutated in one of the resistant clones. The requirement of AMPD3 in LeTx-induced cell death of RAW 264.7 cells was confirmed by the restoration of LeTx sensitivity with ectopic reconstitution of AMPD3 expression. AMPD3 deficiency does not affect LeTx entering cells and the cleavage of mitogen-activated protein kinase kinase (MKK) by lethal factor inside cells, but does impair an unknown downstream event that is linked to cell death. Our data provides new information regarding LeTx-induced macrophage death and suggests that there is a key regulatory site downstream of or parallel to MKK cleavage that controls the cell death in LeTx-treated macrophages.
Insights
AMP deaminase 3 (AMPD3) is crucial for macrophage death during anthrax lethal toxin (LeTx) infection. AMPD3 deficiency protects macrophages from LeTx, revealing a new regulatory pathway in anthrax pathogenesis.
Area of Science:
- Immunology
- Molecular Biology
- Pathogenesis
Background:
- Macrophages are vital for host defense against Bacillus anthracis.
- Macrophage death exacerbates anthrax lethal toxin (LeTx)-induced organ failure.
- Understanding LeTx-induced macrophage death is critical for anthrax treatment.
Purpose of the Study:
- To identify host genes regulating LeTx-induced macrophage cell death.
- To elucidate the molecular mechanisms underlying LeTx cytotoxicity.
- To discover potential therapeutic targets for anthrax.
Main Methods:
- Genetic screening of LeTx-resistant RAW264.7 macrophage mutants.
- Identification of mutated genes using functional assays.
- Confirmation of gene function via gene reconstitution experiments.
Main Results:
- AMP deaminase 3 (AMPD3) was identified as a key gene in LeTx-induced cell death.
- AMPD3 deficiency conferred resistance to LeTx in macrophages.
- AMPD3 is required for a downstream event after MKK cleavage by LeTx, preceding cell death.
Conclusions:
- AMPD3 plays a critical role in LeTx-mediated macrophage apoptosis.
- A novel regulatory pathway downstream of MKK cleavage controls LeTx-induced cell death.
- Targeting AMPD3 or related pathways may offer new strategies against anthrax.
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