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-
1
Hunt NH, Grau GE, 2003. Cytokines: accelerators and brakes in the pathogenesis of cerebral malaria. Trends Immunol 24 :491–499.
-
2
Abraham E, Singer M, 2007. Mechanisms of sepsis-induced organ dysfunction. Crit Care Med 35 :2408–2416.
-
3
Carcillo JA, 2005. Reducing the global burden of sepsis in infants and children: a clinical practice research agenda. Pediatr Crit Care Med 6 :S157–S164.
-
4
van Hensbroek MB, Palmer A, Jaffar S, Schneider G, Kwiatkowski D, 1997. Residual neurologic sequelae after childhood cerebral malaria. J Pediatr 131 :125–129.
-
5
de Souza JB, Riley EM, 2002. Cerebral malaria: the contribution of studies in animal models to our understanding of immunopathogenesis. Microbes Infect 4 :291–300.
-
6
Potter SM, Chan-Ling T, Rosinova E, Ball HJ, Mitchell AJ, Hunt NH, 2006. A role for fas-fas ligand interactions during the late-stage neuropathological processes of experimental cerebral malaria. J Neuroimmunol 173 :96–107.
-
7
Lackner P, Burger C, Pfaller K, Heussler V, Helbok R, Morandell M, Broessner G, Tannich E, Schmutzhard E, Beer R, 2007. Apoptosis in experimental cerebral malaria: spatial profile of cleaved caspase-3 and ultrastructural alterations in different disease stages. Neuropathol Appl Neurobiol 33 :560–571.
-
8
Kim YS, Schwabe RF, Qian T, Lemasters JJ, Brenner DA, 2002. TRAIL-mediated apoptosis requires NF-κB inhibition and the mitochondrial permeability transition in human hepatoma cells. Hepatology 36 :1498–1508.
-
9
Hotchkiss RS, Tinsley KW, Swanson PE, Chang KC, Cobb JP, Buchman TG, Korsmeyer SJ, Karl IE, 1999. Prevention of lymphocyte cell death in sepsis improves survival in mice. Proc Natl Acad Sci USA 96 :14541–14546.
-
10
Chen M, Guerrero AD, Huang L, Shabier Z, Pan M, Tan TH, Wang J, 2007. Caspase-9-induced mitochondrial disruption through cleavage of anti-apoptotic BCL-2 family members. J Biol Chem. 282 :33888–33895.
-
11
Kumar KA, Babu PP, 2002. Mitochondrial anomalies are associated with the induction of intrinsic cell death proteins-bcl(2), bax, cytochrome-c and p53 in mice brain during experimental fatal murine cerebral malaria. Neurosci Lett 329 :319–323.
-
12
Iwata A, Stevenson VM, Minard A, Tasch M, Tupper J, Lagasse E, Weissman I, Harlan JM, Winn RK, 2003. Over-expression of bcl-2 provides protection in septic mice by a transeffect. J Immunol 171 :3136–3141.
-
13
Srivastava A, Henneke P, Visintin A, Morse SC, Martin V, Watkins C, Paton JC, Wessels MR, Golenbock DT, Malley R, 2005. The apoptotic response to pneumolysin is toll-like receptor 4 dependent and protects against pneumococcal disease. Infect Immun 73 :6479–6487.
-
14
Piguet PF, Kan CD, Vesin C, 2002. Thrombocytopenia in an animal model of malaria is associated with an increased caspase-mediated death of thrombocytes. Apoptosis 7 :91–98.
-
15
Pamplona A, Ferreira A, Balla J, Jeney V, Balla G, Epiphanio S, Choral A, Rodrigues CD, Gregoire IP, Cunha-Rodrigues M, Portugal S, Soares MP, Mota MM, 2007. Heme oxygenase-1 and carbon monoxide suppress the pathogenesis of experimental cerebral malaria. Nat Med 13 :703–710.
-
16
Wiessner C, Sauer D, Alaimo D, Allegrini PR, 2000. Protective effect of a caspase inhibitor in models for cerebral ischemia in vitro and in vivo. Cell Mol Biol (Noisy-le-grand) 46 :53–62.
-
17
Park S, Yamaguchi M, Zhou C, Calvert JW, Tang J, Zhang JH, 2004. Neurovascular protection reduces early brain injury after subarachnoid hemorrhage. Stroke 35 :2412–2417.
-
18
Cauwels A, Janssen B, Waeytens A, Cuvelier C, Brouckaert P, 2003. Caspase inhibition causes hyperacute tumor necrosis factor-induced shock via oxidative stress and phospholipase A2. Nat Immunol 4 :387–393.
-
19
Wijsman JH, Jonker RR, Keijzer R, van de Velde CJ, Cornelisse CJ, van Dierendonck JH, 1993. A new method to detect apoptosis in paraffin sections: in situ end-labeling of fragmented DNA. J Histochem Cytochem 41 :7–12.
-
20
Lovegrove FE, Gharib SA, Patel SN, Hawkes CA, Kain KC, Liles WC, 2007. Expression microarray analysis implicates apoptosis and interferon-responsive mechanisms in susceptibility to experimental cerebral malaria. Am J Pathol 171 :1894–1903.
-
21
Farlie PG, Dringen R, Rees SM, Kannourakis G, Bernard O, 1995. Bcl-2 transgene expression can protect neurons against developmental and induced cell death. Proc Natl Acad Sci USA 92 :4397–4401.
-
22
Vandenabeele P, Vanden Berghe T, Festjens N, 2006. Caspase inhibitors promote alternative cell death pathways. Sci STKE 2006 :pe44.
| Past two years | Past Year | Past 30 Days | |
|---|---|---|---|
| Abstract Views | 144 | 107 | 6 |
| Full Text Views | 306 | 3 | 0 |
| PDF Downloads | 47 | 3 | 0 |
Failure of Two Distinct Anti-apoptotic Approaches to Reduce Mortality in Experimental Cerebral Malaria
Andrew J. Helmers
Andrew J. Helmers
Institute of Medical Science, University of Toronto, Toronto, Ontario, Canada; McLaughlin-Rotman Centre for Global Health, McLaughlin Centre for Molecular Medicine, University of Toronto, Toronto, Ontario, Canada; Department of Medicine, University of Washington, Seattle, Washington; Division of Infectious Diseases, Department of Medicine, University of Toronto, Toronto, Ontario, Canada; Toronto General Research Institute, University Health Network, Toronto, Ontario, Canada
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Fiona E. Lovegrove
Fiona E. Lovegrove
Institute of Medical Science, University of Toronto, Toronto, Ontario, Canada; McLaughlin-Rotman Centre for Global Health, McLaughlin Centre for Molecular Medicine, University of Toronto, Toronto, Ontario, Canada; Department of Medicine, University of Washington, Seattle, Washington; Division of Infectious Diseases, Department of Medicine, University of Toronto, Toronto, Ontario, Canada; Toronto General Research Institute, University Health Network, Toronto, Ontario, Canada
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John M. Harlan
John M. Harlan
Institute of Medical Science, University of Toronto, Toronto, Ontario, Canada; McLaughlin-Rotman Centre for Global Health, McLaughlin Centre for Molecular Medicine, University of Toronto, Toronto, Ontario, Canada; Department of Medicine, University of Washington, Seattle, Washington; Division of Infectious Diseases, Department of Medicine, University of Toronto, Toronto, Ontario, Canada; Toronto General Research Institute, University Health Network, Toronto, Ontario, Canada
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Kevin C. Kain
Kevin C. Kain
Institute of Medical Science, University of Toronto, Toronto, Ontario, Canada; McLaughlin-Rotman Centre for Global Health, McLaughlin Centre for Molecular Medicine, University of Toronto, Toronto, Ontario, Canada; Department of Medicine, University of Washington, Seattle, Washington; Division of Infectious Diseases, Department of Medicine, University of Toronto, Toronto, Ontario, Canada; Toronto General Research Institute, University Health Network, Toronto, Ontario, Canada
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W. Conrad Liles
W. Conrad Liles
Institute of Medical Science, University of Toronto, Toronto, Ontario, Canada; McLaughlin-Rotman Centre for Global Health, McLaughlin Centre for Molecular Medicine, University of Toronto, Toronto, Ontario, Canada; Department of Medicine, University of Washington, Seattle, Washington; Division of Infectious Diseases, Department of Medicine, University of Toronto, Toronto, Ontario, Canada; Toronto General Research Institute, University Health Network, Toronto, Ontario, Canada
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Cerebral malaria is responsible for a high proportion of mortality in human Plasmodium falciparum infection. Previous studies have reported the presence of apoptosis in endothelial cells, astrocytes, neurons, and glial cells in experimental murine cerebral malaria caused by infection with Plasmodium berghei ANKA. Using this model, we tested two strategies, which have been shown to improve survival in murine models of sepsis: 1) treatment with z-VAD, a pancaspase inhibitor; and 2) overexpression of Bcl-2 using transgenic mice expressing human Bcl-2 (which prevents the release of apoptotic mediators from the mitochondria) from a myeloid cell promoter. Neither of these anti-apoptotic strategies, previously shown to provide therapeutic benefit in sepsis, improved survival in experimental cerebral malaria.
Author Notes
ProCite
RefWorks
Reference Manager
BibTeX
Zotero
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-
1
Hunt NH, Grau GE, 2003. Cytokines: accelerators and brakes in the pathogenesis of cerebral malaria. Trends Immunol 24 :491–499.
-
2
Abraham E, Singer M, 2007. Mechanisms of sepsis-induced organ dysfunction. Crit Care Med 35 :2408–2416.
-
3
Carcillo JA, 2005. Reducing the global burden of sepsis in infants and children: a clinical practice research agenda. Pediatr Crit Care Med 6 :S157–S164.
-
4
van Hensbroek MB, Palmer A, Jaffar S, Schneider G, Kwiatkowski D, 1997. Residual neurologic sequelae after childhood cerebral malaria. J Pediatr 131 :125–129.
-
5
de Souza JB, Riley EM, 2002. Cerebral malaria: the contribution of studies in animal models to our understanding of immunopathogenesis. Microbes Infect 4 :291–300.
-
6
Potter SM, Chan-Ling T, Rosinova E, Ball HJ, Mitchell AJ, Hunt NH, 2006. A role for fas-fas ligand interactions during the late-stage neuropathological processes of experimental cerebral malaria. J Neuroimmunol 173 :96–107.
-
7
Lackner P, Burger C, Pfaller K, Heussler V, Helbok R, Morandell M, Broessner G, Tannich E, Schmutzhard E, Beer R, 2007. Apoptosis in experimental cerebral malaria: spatial profile of cleaved caspase-3 and ultrastructural alterations in different disease stages. Neuropathol Appl Neurobiol 33 :560–571.
-
8
Kim YS, Schwabe RF, Qian T, Lemasters JJ, Brenner DA, 2002. TRAIL-mediated apoptosis requires NF-κB inhibition and the mitochondrial permeability transition in human hepatoma cells. Hepatology 36 :1498–1508.
-
9
Hotchkiss RS, Tinsley KW, Swanson PE, Chang KC, Cobb JP, Buchman TG, Korsmeyer SJ, Karl IE, 1999. Prevention of lymphocyte cell death in sepsis improves survival in mice. Proc Natl Acad Sci USA 96 :14541–14546.
-
10
Chen M, Guerrero AD, Huang L, Shabier Z, Pan M, Tan TH, Wang J, 2007. Caspase-9-induced mitochondrial disruption through cleavage of anti-apoptotic BCL-2 family members. J Biol Chem. 282 :33888–33895.
-
11
Kumar KA, Babu PP, 2002. Mitochondrial anomalies are associated with the induction of intrinsic cell death proteins-bcl(2), bax, cytochrome-c and p53 in mice brain during experimental fatal murine cerebral malaria. Neurosci Lett 329 :319–323.
-
12
Iwata A, Stevenson VM, Minard A, Tasch M, Tupper J, Lagasse E, Weissman I, Harlan JM, Winn RK, 2003. Over-expression of bcl-2 provides protection in septic mice by a transeffect. J Immunol 171 :3136–3141.
-
13
Srivastava A, Henneke P, Visintin A, Morse SC, Martin V, Watkins C, Paton JC, Wessels MR, Golenbock DT, Malley R, 2005. The apoptotic response to pneumolysin is toll-like receptor 4 dependent and protects against pneumococcal disease. Infect Immun 73 :6479–6487.
-
14
Piguet PF, Kan CD, Vesin C, 2002. Thrombocytopenia in an animal model of malaria is associated with an increased caspase-mediated death of thrombocytes. Apoptosis 7 :91–98.
-
15
Pamplona A, Ferreira A, Balla J, Jeney V, Balla G, Epiphanio S, Choral A, Rodrigues CD, Gregoire IP, Cunha-Rodrigues M, Portugal S, Soares MP, Mota MM, 2007. Heme oxygenase-1 and carbon monoxide suppress the pathogenesis of experimental cerebral malaria. Nat Med 13 :703–710.
-
16
Wiessner C, Sauer D, Alaimo D, Allegrini PR, 2000. Protective effect of a caspase inhibitor in models for cerebral ischemia in vitro and in vivo. Cell Mol Biol (Noisy-le-grand) 46 :53–62.
-
17
Park S, Yamaguchi M, Zhou C, Calvert JW, Tang J, Zhang JH, 2004. Neurovascular protection reduces early brain injury after subarachnoid hemorrhage. Stroke 35 :2412–2417.
-
18
Cauwels A, Janssen B, Waeytens A, Cuvelier C, Brouckaert P, 2003. Caspase inhibition causes hyperacute tumor necrosis factor-induced shock via oxidative stress and phospholipase A2. Nat Immunol 4 :387–393.
-
19
Wijsman JH, Jonker RR, Keijzer R, van de Velde CJ, Cornelisse CJ, van Dierendonck JH, 1993. A new method to detect apoptosis in paraffin sections: in situ end-labeling of fragmented DNA. J Histochem Cytochem 41 :7–12.
-
20
Lovegrove FE, Gharib SA, Patel SN, Hawkes CA, Kain KC, Liles WC, 2007. Expression microarray analysis implicates apoptosis and interferon-responsive mechanisms in susceptibility to experimental cerebral malaria. Am J Pathol 171 :1894–1903.
-
21
Farlie PG, Dringen R, Rees SM, Kannourakis G, Bernard O, 1995. Bcl-2 transgene expression can protect neurons against developmental and induced cell death. Proc Natl Acad Sci USA 92 :4397–4401.
-
22
Vandenabeele P, Vanden Berghe T, Festjens N, 2006. Caspase inhibitors promote alternative cell death pathways. Sci STKE 2006 :pe44.
| Past two years | Past Year | Past 30 Days | |
|---|---|---|---|
| Abstract Views | 144 | 107 | 6 |
| Full Text Views | 306 | 3 | 0 |
| PDF Downloads | 47 | 3 | 0 |