This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Google Scholar
Right arrow Articles by Cardwell, M. M.
Right arrow Articles by Martinez, J. J.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Cardwell, M. M.
Right arrow Articles by Martinez, J. J.

 Previous Article  |  Next Article 

Infection and Immunity, December 2009, p. 5272-5280, Vol. 77, No. 12
0019-9567/09/$08.00+0     doi:10.1128/IAI.00201-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

The Sca2 Autotransporter Protein from Rickettsia conorii Is Sufficient To Mediate Adherence to and Invasion of Cultured Mammalian Cells{triangledown}

Marissa M. Cardwell and Juan J. Martinez*

The University of Chicago, The Department of Microbiology, 920 East 58th Street, Cummings Life Sciences Center 707A, Chicago, Illinois 60637

Received 20 February 2009/ Returned for modification 18 March 2009/ Accepted 24 September 2009

Obligate intracellular bacteria of the genus Rickettsia must adhere to and invade the host endothelium in order to establish an infection. These processes require the interaction of rickettsial surface proteins with mammalian host cell receptors. A previous bioinformatic analysis of sequenced rickettsial species identified a family of at least 17 predicted "surface cell antigen" (sca) genes whose products resemble autotransporter proteins. Two members of this family, rOmpA and rOmpB of spotted fever group (SFG) rickettsiae have been identified as adhesion and invasion factors, respectively; however, little is known about the putative functions of the other sca gene products. An intact sca2 gene is found in the majority of pathogenic SFG rickettsiae and, due to its sequence conservation among these species, we predict that Sca2 may play an important function at the rickettsial surface. Here we have shown that sca2 is transcribed and expressed in Rickettsia conorii and have used a heterologous gain-of-function assay in E. coli to determine the putative role of Sca2. Using this system, we have demonstrated that expression of Sca2 at the outer membrane of nonadherent, noninvasive E. coli is sufficient to mediate adherence to and invasion of a panel of mammalian cells, including endothelial cells. Furthermore, soluble Sca2 protein is capable of diminishing R. conorii invasion of cultured mammalian cells. This is the first evidence that Sca2 participates in the interaction between SFG rickettsiae and host cells and suggests that in addition to other surface proteins, Sca2 may play a critical role in rickettsial pathogenesis.

* Corresponding author. Mailing address: The University of Chicago, The Department of Microbiology, 920 East 58th Street, Cummings Life Sciences Center 707A, Chicago, IL 60637. Phone: (773) 834-4556. Fax: (773) 834-8150. E-mail: jmartine{at}bsd.uchicago.edu

{triangledown} Published ahead of print on 5 October 2009.

Editor: R. P. Morrison

Infection and Immunity, December 2009, p. 5272-5280, Vol. 77, No. 12
0019-9567/09/$08.00+0     doi:10.1128/IAI.00201-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»