J Med Microbiol Track the topics, authors and articles important to you
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


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
Right arrow Citation Map
Services
Right arrow Email this article to a friend
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 arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Townsend, S. M.
Right arrow Articles by Badger, J. L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Townsend, S. M.
Right arrow Articles by Badger, J. L.
Agricola
Right arrow Articles by Townsend, S. M.
Right arrow Articles by Badger, J. L.
J Med Microbiol 55 (2006), 1631-1640; DOI: 10.1099/jmm.0.46596-0
© 2006 Society for General Microbiology
ISSN 1473-5644

fliP influences Citrobacter koseri macrophage uptake, cytokine expression and brain abscess formation in the neonatal rat

Stacy M. Townsend1,{dagger}, Ignacio Gonzalez-Gomez1,2 and Julie L. Badger1,2

Department of Pathology, Childrens Hospital Los Angeles1 and University of Southern California Keck School of Medicine, Los Angeles2 , CA 90027, USA

Correspondence
Stacy M. Townsend
stacy.townsend{at}ntu.ac.uk

Received 27 February 2006
Accepted 8 August 2006


Citrobacter koseri causes neonatal meningitis frequently complicated with multiple brain abscesses. During C. koseri central nervous system infection in the neonatal rat model, previous studies have documented many bacteria-filled macrophages within the neonatal rat brain and abscesses. Previous studies have also shown that C. koseri is taken up by, survives phagolysosomal fusion and replicates in macrophages in vitro and in vivo. In this study, in order to elucidate genetic and cellular factors contributing to C. koseri persistence, a combinatory technique of differential fluorescence induction and transposon mutagenesis was employed to isolate C. koseri genes induced while inside macrophages. Several banks of mutants were subjected to a series of enrichments to select for gfp : : transposon fusion into genes that are turned off in vitro but expressed when intracellular within macrophages. Further screening identified several mutants attenuated in their recovery from macrophages compared with the wild-type. A mutation within an Escherichia coli fliP homologue caused significant attenuation in uptake and hypervirulence in vivo, resulting in death within 24 h. Furthermore, analysis of the immunoregulatory interleukin (IL)-10/IL-12 cytokine response during infection suggested that C. koseri fliP expression may alter this response. A better understanding of the bacteria–macrophage interaction at the molecular level and its contribution to brain abscess formation will assist in developing preventative and therapeutic strategies.


Abbreviations: CNS, central nervous system; CSF, cerebrospinal fluid; FACS, fluorescence activated cell sort; i.c., intracranial; IL, interleukin; i.p., intraperitoneal; PMA, phorbol 12-myristate 13-acetate.

The GenBank/EMBL/DDBJ accession number for the fliP sequence of Citrobacter koseri mutant SMT350 determined in this study is DQ233671.

{dagger}Present address: School of Biomedical and Natural Sciences, The Nottingham Trent University, Clifton Lane, Nottingham NG11 8NS, UK.







HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
INT J SYST EVOL MICROBIOL J MED MICROBIOL MICROBIOLOGY J GEN VIROL ALL SGM JOURNALS
Copyright © 2006 Society for General Microbiology.