IAI FigSearch
Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
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
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Falzano, L.
Right arrow Articles by Fiorentini, C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Falzano, L.
Right arrow Articles by Fiorentini, C.

 Previous Article  |  Next Article 

Infection and Immunity, July 2003, p. 4178-4181, Vol. 71, No. 7
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.7.4178-4181.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Cytotoxic Necrotizing Factor 1 Enhances Reactive Oxygen Species-Dependent Transcription and Secretion of Proinflammatory Cytokines in Human Uroepithelial Cells

Loredana Falzano,1 Maria Giovanna Quaranta,2 Sara Travaglione,1 Perla Filippini,1 Alessia Fabbri,1 Marina Viora,2 Gianfranco Donelli,1 and Carla Fiorentini1*

Department of Ultrastructures,1 Department of Immunology, Istituto Superiore di Sanità, 00161 Rome, Italy2

Received 16 December 2002/ Returned for modification 27 January 2003/ Accepted 28 March 2003

Uropathogenic Escherichia coli strains frequently produce a Rho-activating protein toxin named cytotoxic necrotizing factor type 1 (CNF1). We herein report that CNF1 promotes transcription and release of tumor necrosis factor alpha, gamma interferon, interleukin-6 (IL-6), and IL-8 proinflammatory cytokines and increases the production of reactive oxygen species (ROS) in uroepithelial T24 cells. The antioxidant N-acetyl-L-cysteine counteracts these phenomena, a fact which suggests a role for ROS-mediated signaling in CNF1-induced proinflammatory cytokine production.


* Corresponding author. Mailing address: Department of Ultrastructures, Viale Regina Elena 299, 00161 Rome, Italy. Phone: 39 06 49903006. Fax: 39 06 49387140. E-mail: carla.fiorentini{at}iss.it.

Editor: F. C. Fang


Infection and Immunity, July 2003, p. 4178-4181, Vol. 71, No. 7
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.7.4178-4181.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.




This article has been cited by other articles:




Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
J. Bacteriol. J. Virol. Eukaryot. Cell
Microbiol. Mol. Biol. Rev. Clin. Vaccine Immunol. All ASM Journals

Copyright © 2003 by the American Society for Microbiology. All rights reserved.