scholarly journals Mechanism of splenic cell death and host mortality in a Plasmodium yoelii malaria model

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Norinne Lacerda-Queiroz ◽  
Nicolas Riteau ◽  
Richard T. Eastman ◽  
Kevin W. Bock ◽  
Marlene S. Orandle ◽  
...  
Keyword(s):  
Cell Death ◽  
Plasmodium Yoelii ◽  
Splenic Cell ◽  
Host Mortality ◽  
Malaria Model

Antimalarial efficacy, cytotoxicity, and genotoxicity of methanolic stem bark extract from Hintonia latiflora in a Plasmodium yoelii yoelii lethal murine malaria model

2014 ◽  
Vol 113 (4) ◽  
pp. 1529-1536 ◽  
Author(s):  
Norma Rivera ◽  
Perla Y. López ◽  
Marcela Rojas ◽  
Teresa I. Fortoul ◽  
Diana Y. Reynada ◽  
...  
Keyword(s):  
Stem Bark ◽  
Plasmodium Yoelii ◽  
Bark Extract ◽  
Stem Bark Extract ◽  
Plasmodium Yoelii Yoelii ◽  
Malaria Model

Nanoparticle formulation enhanced protective immunity provoked by PYGPI8p-transamidase related protein (PyTAM) DNA vaccine in Plasmodium yoelii malaria model

Vaccine ◽  
2014 ◽  
Vol 32 (17) ◽  
pp. 1998-2006 ◽  
Author(s):  
Mahamoud Sama Cherif ◽  
Mohammed Nasir Shuaibu ◽  
Yukinobu Kodama ◽  
Tomoaki Kurosaki ◽  
Gideon Kofi Helegbe ◽  
...  
Keyword(s):  
Dna Vaccine ◽  
Protective Immunity ◽  
Plasmodium Yoelii ◽  
Related Protein ◽  
Nanoparticle Formulation ◽  
Malaria Model

An efficient strategy for gene targeting and phenotypic assessment in the Plasmodium yoelii rodent malaria model

2008 ◽  
Vol 158 (2) ◽  
pp. 213-216 ◽  
Author(s):  
Sebastian A. Mikolajczak ◽  
Ahmed S.I. Aly ◽  
Ronald F. Dumpit ◽  
Ashley M. Vaughan ◽  
Stefan H.I. Kappe
Keyword(s):  
Gene Targeting ◽  
Plasmodium Yoelii ◽  
Rodent Malaria ◽  
Efficient Strategy ◽  
Malaria Model

scholarly journals Disseminated Candidiasis and Hepatic Malarial Infection in Mannose-Binding-Lectin-A-Deficient Mice

2002 ◽  
Vol 22 (23) ◽  
pp. 8199-8203 ◽  
Author(s):  
Sena J. Lee ◽  
Gloria Gonzalez-Aseguinolaza ◽  
Michel C. Nussenzweig
Keyword(s):  
Survival Rates ◽  
Plasmodium Yoelii ◽  
Mannose Binding Lectin ◽  
Microbial Pathogens ◽  
Mouse Strains ◽  
Disseminated Candidiasis ◽  
Mannose Binding ◽  
Hepatic Invasion ◽  
Malaria Model ◽  
Binding Lectin

ABSTRACT To examine the physiological functions of mannose-binding lectin A (MBL-A), we generated mice that were deficient in MBL-A and examined their susceptibilities to the microbial pathogens Candida albicans and Plasmodium yoelii, an accepted experimental malaria model in mouse. We found no differences in the survival rates and fungal burdens of wild-type and MBL-A−/− mice with disseminated C. albicans infection. The two mouse strains were also similar in their abilities to resist hepatic accumulation of P. yoelii parasites. We conclude that MBL-A deficiency does not alter resistance to disseminated candidiasis or initial hepatic invasion by P. yoelii.

Malaria parasite induces tryptophan-related immune suppression in mice

Parasitology ◽  
2007 ◽  
Vol 134 (7) ◽  
pp. 923-930 ◽  
Author(s):  
K. TETSUTANI ◽  
H. TO ◽  
M. TORII ◽  
H. HISAEDA ◽  
K. HIMENO
Keyword(s):  
Biological Significance ◽  
Plasmodium Yoelii ◽  
Tryptophan Depletion ◽  
Malaria Parasites ◽  
Host Immune Responses ◽  
Tryptophan Catabolism ◽  
Ifn Γ ◽  
Rate Limiting ◽  
Malaria Model

SUMMARYPlasmodium spp. cause the worst parasitic diseases in humans and evade host immunity in complicated ways. Activated catabolism of tryptophan in dendritic cells is thought to suppress immunity, which is mediated by an inducible rate-limiting enzyme of tryptophan catabolism, indoleamine 2,3 dioxygenase (IDO), via both tryptophan depletion and production of toxic metabolites. In various infections, including malaria, IDO is known to be activated but its biological significance is unclear; therefore, we investigated whether malaria parasites induce IDO to suppress host immune responses. We found that enzymatic activity of IDO was elevated systematically in our mouse malaria model, and was abolished by in vivo IDO inhibition with 1-methyl tryptophan. Experimental infection with Plasmodium yoelii showed that IDO inhibition slightly suppressed parasite density in association with enhanced proliferation and IFN-γ production by CD4+ T cells in response to malaria parasites. Our observations suggest that induction of IDO is one of the immune mechanisms of malaria parasites.

DNA nick end labeling: a reliable marker for apoptosis?

1995 ◽  
Vol 53 ◽  
pp. 962-963
Author(s):  
Anne F. Bushnell ◽  
Sarah Webster ◽  
Lynn S. Perlmutter
Keyword(s):  
Cell Death ◽  
Cultured Cells ◽  
Apoptotic Cell ◽  
Morphological Characteristics ◽  
Detection Methods ◽  
Tissue Preparation ◽  
Preparation Methods ◽  
Dna Laddering ◽  
Disease States ◽  
Reliable Marker

Apoptosis, or programmed cell death, is an important mechanism in development and in diverse disease states. The morphological characteristics of apoptosis were first identified using the electron microscope. Since then, DNA laddering on agarose gels was found to correlate well with apoptotic cell death in cultured cells of dissimilar origins. Recently numerous DNA nick end labeling methods have been developed in an attempt to visualize, at the light microscopic level, the apoptotic cells responsible for DNA laddering.The present studies were designed to compare various tissue processing techniques and staining methods to assess the occurrence of apoptosis in post mortem tissue from Alzheimer's diseased (AD) and control human brains by DNA nick end labeling methods. Three tissue preparation methods and two commercial DNA nick end labeling kits were evaluated: the Apoptag kit from Oncor and the Biotin-21 dUTP 3' end labeling kit from Clontech. The detection methods of the two kits differed in that the Oncor kit used digoxigenin dUTP and anti-digoxigenin-peroxidase and the Clontech used biotinylated dUTP and avidinperoxidase. Both used 3-3' diaminobenzidine (DAB) for final color development.

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