Document Detail


The acid phosphatase AcpA is secreted in vitro and in macrophages by Francisella spp.
MedLine Citation:
PMID:  22184418     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Francisella tularensis is a remarkably infectious facultative intracellular pathogen that causes the zoonotic disease tularemia. Essential to the pathogenesis of F. tularensis is its ability to escape the destructive phagosomal environment and inhibit the host cell respiratory burst. F. tularensis subspecies encode a series of acid phosphatases, which have been reported to play important roles in Francisella phagosomal escape, inhibition of the respiratory burst, and intracellular survival. However, rigorous demonstration of acid phosphatase secretion by intracellular Francisella has not been shown. Here, we demonstrate that AcpA, which contributes most of the F. tularensis acid phosphatase activity, is secreted into the culture supernatant in vitro by F. novicida and F. tularensis subsp. holarctica LVS. In addition, both F. novicida and the highly virulent F. tularensis subsp. tularensis Schu S4 strain are able to secrete and also translocate AcpA into the host macrophage cytosol. This is the first evidence of acid phosphatase translocation during macrophage infection, and this knowledge will greatly enhance our understanding of the functions of these enzymes in Francisella pathogenesis.
Authors:
Shipan Dai; Nrusingh P Mohapatra; Larry S Schlesinger; John S Gunn
Related Documents :
3160948 - Identification of mutagenic compounds formed during chlorination of humic acid.
399918 - Mutagenicity of resin acids identified in pulp and paper mill effluents using the salmo...
7821298 - Chemical and mutagenic patterns of airborne particulate matter collected in 17 italian ...
19696918 - Effect of organic acids on escherichia coli o157:h7 and staphylococcus aureus contamina...
24712818 - Dielectric spectra broadening as a signature for dipole-matrix interaction. iv. water i...
16348608 - Nitrification at low ph by aggregated chemolithotrophic bacteria.
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2011-12-19
Journal Detail:
Title:  Infection and immunity     Volume:  80     ISSN:  1098-5522     ISO Abbreviation:  Infect. Immun.     Publication Date:  2012 Mar 
Date Detail:
Created Date:  2012-02-16     Completed Date:  2012-04-09     Revised Date:  2013-06-26    
Medline Journal Info:
Nlm Unique ID:  0246127     Medline TA:  Infect Immun     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1088-97     Citation Subset:  IM    
Affiliation:
Center for Microbial Interface Biology, Department of Microbial Infection and Immunity, The Ohio State University, Columbus, Ohio, USA.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Acid Phosphatase / secretion*
Animals
Cells, Cultured
Francisella tularensis / enzymology*,  pathogenicity*
Humans
Macrophages / microbiology*
Protein Transport
Virulence Factors / metabolism*
Grant Support
ID/Acronym/Agency:
2-U54-AI-057153/AI/NIAID NIH HHS
Chemical
Reg. No./Substance:
0/Virulence Factors; EC 3.1.3.2/Acid Phosphatase
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Competition and resilience between founder and introduced bacteria in the Caenorhabditis elegans gut...
Next Document:  Phenotypic characterization of a copA mutant of Neisseria gonorrhoeae identifies a link between copp...