Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
2009-11-16
pubmed:abstractText
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.
pubmed:grant
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/19805531-10318762, http://linkedlifedata.com/resource/pubmed/commentcorrection/19805531-10856226, http://linkedlifedata.com/resource/pubmed/commentcorrection/19805531-15039346, http://linkedlifedata.com/resource/pubmed/commentcorrection/19805531-15073367, http://linkedlifedata.com/resource/pubmed/commentcorrection/19805531-15155660, http://linkedlifedata.com/resource/pubmed/commentcorrection/19805531-15383620, http://linkedlifedata.com/resource/pubmed/commentcorrection/19805531-15590781, http://linkedlifedata.com/resource/pubmed/commentcorrection/19805531-16360032, http://linkedlifedata.com/resource/pubmed/commentcorrection/19805531-16500128, http://linkedlifedata.com/resource/pubmed/commentcorrection/19805531-16504018, http://linkedlifedata.com/resource/pubmed/commentcorrection/19805531-1729180, http://linkedlifedata.com/resource/pubmed/commentcorrection/19805531-19134120, http://linkedlifedata.com/resource/pubmed/commentcorrection/19805531-1916232, http://linkedlifedata.com/resource/pubmed/commentcorrection/19805531-3192207, http://linkedlifedata.com/resource/pubmed/commentcorrection/19805531-3885774, http://linkedlifedata.com/resource/pubmed/commentcorrection/19805531-5424499, http://linkedlifedata.com/resource/pubmed/commentcorrection/19805531-6407019, http://linkedlifedata.com/resource/pubmed/commentcorrection/19805531-8286624, http://linkedlifedata.com/resource/pubmed/commentcorrection/19805531-8805076, http://linkedlifedata.com/resource/pubmed/commentcorrection/19805531-9600861
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1098-5522
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
77
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
5272-80
pubmed:dateRevised
2010-9-28
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
The Sca2 autotransporter protein from Rickettsia conorii is sufficient to mediate adherence to and invasion of cultured mammalian cells.
pubmed:affiliation
The Department of Microbiology, The University of Chicago, Cummings Life Sciences Center 707A, Chicago, Illinois 60637, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural