Abstract
Escherichia coli hemolysin is the prototype of a large family of pore-forming toxins produced by gram-negative organisms. Besides its known cytotoxic activities against granulocytes, monocytes, endothelial cells, and renal epithelial cells, we now demonstrate that the toxin potently kills human T lymphocytes. Evidence based on different and independent approaches indicates that lymphocidal activity is due to formation of transmembrane pores. Additionally, cells prestimulated with phytohemagglutinin respond to low doses of E. coli hemolysin with DNA fragmentation similar to that observed in cells undergoing programmed cell death. Kinetic considerations lead us to conclude that DNA degradation may, however, represent an epiphenomenon. Killing of T cells is another means through which E. coli hemolysin could directly impair host defense.
MeSH Terms
Adenosine Triphosphate/metabolism
Cell Death/drug effects
Cell Membrane Permeability/drug effects
DNA/drug effects
DNA Damage
Dose-Response Relationship, Drug
Escherichia coli/pathogenicity
Hemolysin Proteins/toxicity
Humans
In Vitro Techniques
Lymphocyte Activation/drug effects
T-Lymphocytes/drug effects
Time Factors
Chemicals
Hemolysin Proteins
Adenosine Triphosphate
DNA
Authors & Affiliations
5 authors, click to expand affiliations / ORCID
Jonas D
Institute of Medical Microbiology, University of Mainz, Germany.
Schultheis B
Klas C
Krammer P H
Bhakdi S
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