Document Detail


Three Yersinia pestis adhesins facilitate Yop delivery to eukaryotic cells and contribute to plague virulence.
MedLine Citation:
PMID:  20679446     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
To establish a successful infection, Yersinia pestis requires the delivery of cytotoxic Yops to host cells. Yops inhibit phagocytosis, block cytokine responses, and induce apoptosis of macrophages. The Y. pestis adhesin Ail facilitates Yop translocation and is required for full virulence in mice. To determine the contributions of other adhesins to Yop delivery, we deleted five known adhesins of Y. pestis. In addition to Ail, plasminogen activator (Pla) and pH 6 antigen (Psa) could mediate Yop translocation to host cells. The contribution of each adhesin to binding and Yop delivery was dependent upon the growth conditions. When cells were pregrown at 28°C and pH 7, the order of importance for adhesins in cell binding and cytotoxicity was Ail > Pla > Psa. Y. pestis grown at 37°C and pH 7 had equal contributions from Ail and Pla but an undetectable role for Psa. At 37°C and pH 6, both Ail and Psa contributed to binding and Yop delivery, while Pla contributed minimally. Pla-mediated Yop translocation was independent of protease activity. Of the three single mutants, the Δail mutant was the most defective in mouse virulence. The expression level of ail was also the highest of the three adhesins in infected mouse tissues. Compared to an ail mutant, additional deletion of psaA (encoding Psa) led to a 130,000-fold increase in the 50% lethal dose for mice relative to that of the KIM5 parental strain. Our results indicate that in addition to Ail, Pla and Psa can serve as environmentally specific adhesins to facilitate Yop secretion, a critical virulence function of Y. pestis.
Authors:
Suleyman Felek; Tiffany M Tsang; Eric S Krukonis
Related Documents :
19919566 - Recent insights into host-pathogen interactions from dictyostelium.
15470236 - Transcriptional response of candida albicans upon internalization by macrophages.
15808306 - Molecular analyses of disease pathogenesis: application of bovine microarrays.
20976286 - T-cell subsets and antifungal host defenses.
17045986 - Lymphatic regeneration across an incisional wound: inhibition by dexamethasone and aspi...
22498766 - Regulatory t cells in atherogenesis.
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-08-02
Journal Detail:
Title:  Infection and immunity     Volume:  78     ISSN:  1098-5522     ISO Abbreviation:  Infect. Immun.     Publication Date:  2010 Oct 
Date Detail:
Created Date:  2010-09-22     Completed Date:  2010-11-12     Revised Date:  2011-07-27    
Medline Journal Info:
Nlm Unique ID:  0246127     Medline TA:  Infect Immun     Country:  United States    
Other Details:
Languages:  eng     Pagination:  4134-50     Citation Subset:  IM    
Affiliation:
Department of Biologic and Materials Sciences, University of Michigan School of Dentistry, Ann Arbor, MI 48109-1078, USA.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Adhesins, Bacterial / metabolism*
Animals
Bacterial Adhesion / physiology
Cell Line
Female
Gene Expression Regulation, Bacterial / physiology
Humans
Membrane Proteins / metabolism*
Mice
Mutation
Plague / microbiology*
Virulence
Yersinia pestis / metabolism*,  pathogenicity*
Chemical
Reg. No./Substance:
0/Adhesins, Bacterial; 0/Membrane Proteins
Comments/Corrections

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


Previous Document:  Staphylococcus aureus lipoprotein SitC co-localizes with TLR2 in murine keratinocytes and elicits in...
Next Document:  Viscoelasticity-based Staging of Hepatic Fibrosis with Multifrequency MR Elastography.