Document Detail


The Trypanosoma cruzi protease cruzain mediates immune evasion.
MedLine Citation:
PMID:  21909255     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Trypanosoma cruzi is the causative agent of Chagas' disease. Novel chemotherapy with the drug K11777 targets the major cysteine protease cruzain and disrupts amastigote intracellular development. Nevertheless, the biological role of the protease in infection and pathogenesis remains unclear as cruzain gene knockout failed due to genetic redundancy. A role for the T. cruzi cysteine protease cruzain in immune evasion was elucidated in a comparative study of parental wild type- and cruzain-deficient parasites. Wild type T. cruzi did not activate host macrophages during early infection (<60 min) and no increase in ∼P iκB was detected. The signaling factor NF-κB P65 colocalized with cruzain on the cell surface of intracellular wild type parasites, and was proteolytically cleaved. No significant IL-12 expression occurred in macrophages infected with wild type T. cruzi and treated with LPS and BFA, confirming impairment of macrophage activation pathways. In contrast, cruzain-deficient parasites induced macrophage activation, detectable iκB phosphorylation, and nuclear NF-κB P65 localization. These parasites were unable to develop intracellularly and survive within macrophages. IL 12 expression levels in macrophages infected with cruzain-deficient T. cruzi were comparable to LPS activated controls. Thus cruzain hinders macrophage activation during the early (<60 min) stages of infection, by interruption of the NF-κB P65 mediated signaling pathway. These early events allow T. cruzi survival and replication, and may lead to the spread of infection in acute Chagas' disease.
Authors:
Patricia S Doyle; Yuan M Zhou; Ivy Hsieh; Doron C Greenbaum; James H McKerrow; Juan C Engel
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2011-09-01
Journal Detail:
Title:  PLoS pathogens     Volume:  7     ISSN:  1553-7374     ISO Abbreviation:  PLoS Pathog.     Publication Date:  2011 Sep 
Date Detail:
Created Date:  2011-09-12     Completed Date:  2012-01-05     Revised Date:  2012-04-26    
Medline Journal Info:
Nlm Unique ID:  101238921     Medline TA:  PLoS Pathog     Country:  United States    
Other Details:
Languages:  eng     Pagination:  e1002139     Citation Subset:  IM    
Affiliation:
Tropical Disease Research Unit and Sandler Center for Drug Discovery, Department of Pathology, University of California, San Francisco, California, United States of America.
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MeSH Terms
Descriptor/Qualifier:
Animals
Arginase / biosynthesis
Cysteine Endopeptidases / deficiency,  physiology*
Dipeptides / pharmacology
Humans
I-kappa B Proteins / metabolism
Immune Evasion / physiology*
Interleukin-12 / biosynthesis
Lipopolysaccharides / pharmacology
Macrophage Activation / drug effects
Macrophages / drug effects,  metabolism,  parasitology*
Mice
NF-kappa B / metabolism
Protozoan Proteins / physiology*
Trypanosoma cruzi / drug effects,  genetics
Vinyl Compounds / pharmacology
Grant Support
ID/Acronym/Agency:
AI 35707/AI/NIAID NIH HHS
Chemical
Reg. No./Substance:
0/Dipeptides; 0/I-kappa B Proteins; 0/Lipopolysaccharides; 0/N-pip-phenylalanine-homophenylalanine-vinyl sulfone phenyl; 0/NF-kappa B; 0/Protozoan Proteins; 0/Vinyl Compounds; 187348-17-0/Interleukin-12; EC 3.4.22.-/Cysteine Endopeptidases; EC 3.4.22.-/cruzain, Trypanosoma cruzi; EC 3.5.3.1/Arginase
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