Pneumolysin Causes Neuronal Cell Death through Mitochondrial Damage

Bacterial toxins such as pneumolysin are key mediators of cytotoxicity in infections. Pneumolysin is a pore-forming toxin released by Streptococcus pneumoniae, the major cause of bacterial meningitis. We found that pneumolysin is the pneumococcal factor that accounts for the cell death pathways indu...

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Published inInfection and Immunity Vol. 75; no. 9; pp. 4245 - 4254
Main Authors Braun, Johann S, Hoffmann, Olaf, Schickhaus, Miriam, Freyer, Dorette, Dagand, Emilie, Bermpohl, Daniela, Mitchell, Tim J, Bechmann, Ingo, Weber, Joerg R
Format Journal Article
LanguageEnglish
Published Washington, DC American Society for Microbiology 01.09.2007
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Abstract Bacterial toxins such as pneumolysin are key mediators of cytotoxicity in infections. Pneumolysin is a pore-forming toxin released by Streptococcus pneumoniae, the major cause of bacterial meningitis. We found that pneumolysin is the pneumococcal factor that accounts for the cell death pathways induced by live bacteria in primary neurons. The pore-forming activity of pneumolysin is essential for the induction of mitochondrial damage and apoptosis. Pneumolysin colocalized with mitochondrial membranes, altered the mitochondrial membrane potential, and caused the release of apoptosis-inducing factor and cell death. Pneumolysin induced neuronal apoptosis without activating caspase-1, -3, or -8. Wild-type pneumococci also induced apoptosis without activation of caspase-3, whereas pneumolysin-negative pneumococci activated caspase-3 through the release of bacterial hydrogen peroxide. Pneumolysin caused upregulation of X-chromosome-linked inhibitor of apoptosis protein and inhibited staurosporine-induced caspase activation, suggesting the presence of actively suppressive mechanisms on caspases. In conclusion, our results indicate additional functions of pneumolysin as a mitochondrial toxin and as a determinant of caspase-independent apoptosis. Considering this, blocking of pneumolysin may be a promising cytoprotective strategy in pneumococcal meningitis and other infections.
AbstractList Bacterial toxins such as pneumolysin are key mediators of cytotoxicity in infections. Pneumolysin is a pore-forming toxin released by Streptococcus pneumoniae , the major cause of bacterial meningitis. We found that pneumolysin is the pneumococcal factor that accounts for the cell death pathways induced by live bacteria in primary neurons. The pore-forming activity of pneumolysin is essential for the induction of mitochondrial damage and apoptosis. Pneumolysin colocalized with mitochondrial membranes, altered the mitochondrial membrane potential, and caused the release of apoptosis-inducing factor and cell death. Pneumolysin induced neuronal apoptosis without activating caspase-1, -3, or -8. Wild-type pneumococci also induced apoptosis without activation of caspase-3, whereas pneumolysin-negative pneumococci activated caspase-3 through the release of bacterial hydrogen peroxide. Pneumolysin caused upregulation of X-chromosome-linked inhibitor of apoptosis protein and inhibited staurosporine-induced caspase activation, suggesting the presence of actively suppressive mechanisms on caspases. In conclusion, our results indicate additional functions of pneumolysin as a mitochondrial toxin and as a determinant of caspase-independent apoptosis. Considering this, blocking of pneumolysin may be a promising cytoprotective strategy in pneumococcal meningitis and other infections.
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Bacterial toxins such as pneumolysin are key mediators of cytotoxicity in infections. Pneumolysin is a pore-forming toxin released by Streptococcus pneumoniae, the major cause of bacterial meningitis. We found that pneumolysin is the pneumococcal factor that accounts for the cell death pathways induced by live bacteria in primary neurons. The pore-forming activity of pneumolysin is essential for the induction of mitochondrial damage and apoptosis. Pneumolysin colocalized with mitochondrial membranes, altered the mitochondrial membrane potential, and caused the release of apoptosis-inducing factor and cell death. Pneumolysin induced neuronal apoptosis without activating caspase-1, -3, or -8. Wild-type pneumococci also induced apoptosis without activation of caspase-3, whereas pneumolysin-negative pneumococci activated caspase-3 through the release of bacterial hydrogen peroxide. Pneumolysin caused upregulation of X-chromosome-linked inhibitor of apoptosis protein and inhibited staurosporine-induced caspase activation, suggesting the presence of actively suppressive mechanisms on caspases. In conclusion, our results indicate additional functions of pneumolysin as a mitochondrial toxin and as a determinant of caspase-independent apoptosis. Considering this, blocking of pneumolysin may be a promising cytoprotective strategy in pneumococcal meningitis and other infections.
Author Mitchell, Tim J
Bermpohl, Daniela
Braun, Johann S
Bechmann, Ingo
Hoffmann, Olaf
Schickhaus, Miriam
Weber, Joerg R
Freyer, Dorette
Dagand, Emilie
AuthorAffiliation Departments of Neurology, 1 Cell Biology and Neurobiology, Charité Universitaetsmedizin Berlin, Berlin, Germany, 2 Division of Neurology, Department of Internal Medicine, Faculty of Medicine and Health Sciences, United Arab Emirates University, Al Ain, United Arab Emirates, 3 Division of Infection and Immunity, University of Glasgow, Glasgow, United Kingdom 4
AuthorAffiliation_xml – name: Departments of Neurology, 1 Cell Biology and Neurobiology, Charité Universitaetsmedizin Berlin, Berlin, Germany, 2 Division of Neurology, Department of Internal Medicine, Faculty of Medicine and Health Sciences, United Arab Emirates University, Al Ain, United Arab Emirates, 3 Division of Infection and Immunity, University of Glasgow, Glasgow, United Kingdom 4
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Corresponding author. Mailing address: United Arab Emirates University, Faculty of Medicine and Health Sciences, Department of Internal Medicine, Division of Neurology, P.O. Box 17666, Al Ain, United Arab Emirates. Phone: 971 3 7137 419. Fax: 971 3 7672 995. E-mail: johannb@uaeu.ac.ae
J.S.B. and O.H. contributed equally to this work.
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Snippet Bacterial toxins such as pneumolysin are key mediators of cytotoxicity in infections. Pneumolysin is a pore-forming toxin released by Streptococcus pneumoniae,...
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Bacterial toxins such as pneumolysin are key mediators of cytotoxicity in infections. Pneumolysin is a pore-forming toxin released by Streptococcus pneumoniae...
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StartPage 4245
SubjectTerms Animals
Antineoplastic agents
Apoptosis - physiology
Bacterial Proteins - physiology
Biological and medical sciences
Calcium - metabolism
Cell Death - physiology
Cells, Cultured
Cellular Microbiology: Pathogen-Host Cell Molecular Interactions
Chemotherapy
Medical sciences
Membrane Potential, Mitochondrial - physiology
Mitochondria - metabolism
Mitochondria - microbiology
Mitochondria - pathology
Mitochondrial Membranes - microbiology
Mitochondrial Membranes - pathology
Neurons - metabolism
Neurons - microbiology
Neurons - pathology
Pharmacology. Drug treatments
Rats
Reactive Oxygen Species - metabolism
Signal Transduction - physiology
Streptococcus pneumoniae
Streptococcus pneumoniae - pathogenicity
Streptolysins - physiology
Up-Regulation - physiology
Title Pneumolysin Causes Neuronal Cell Death through Mitochondrial Damage
URI http://iai.asm.org/content/75/9/4245.abstract
https://www.ncbi.nlm.nih.gov/pubmed/17562768
https://search.proquest.com/docview/20995178
https://search.proquest.com/docview/68180863
https://pubmed.ncbi.nlm.nih.gov/PMC1951198
Volume 75
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