J Med Microbiol Email Content Delivery
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 Mattar, R.
Right arrow Articles by Carrilho, F. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Mattar, R.
Right arrow Articles by Carrilho, F. J.
Agricola
Right arrow Articles by Mattar, R.
Right arrow Articles by Carrilho, F. J.
J Med Microbiol 56 (2007), 9-14; DOI: 10.1099/jmm.0.46824-0
© 2007 Society for General Microbiology
ISSN 1473-5644

Helicobacter pylori cag pathogenicity island genes: clinical relevance for peptic ulcer disease development in Brazil

Rejane Mattar, Sergio Barbosa Marques, Maria do Socorro Monteiro, Anibal Ferreira dos Santos, Kiyoshi Iriya and Flair José Carrilho

Department of Gastroenterology, University of São Paulo School of Medicine, São Paulo, SP, Brazil

Correspondence
Rejane Mattar
rmattar{at}hcnet.usp.br or
rejane-mattar{at}ig.com.br

Received 7 July 2006
Accepted 28 August 2006


The purpose of this study was to verify whether the presence of any of the Helicobacter pylori cagPAI genes or segments – cagA, cagA promoter, cagE, cagM, tnpB, tnpA, cagT and the left end of the cag II (LEC) region – would be a useful marker for the risk of peptic ulcer disease development. H. pylori DNA extracted from positive urease tests of 150 peptic ulcer patients and 65 dyspeptic controls was analysed by PCR. Duodenal ulcers were present in 110, gastric ulcers in 23 and both gastric and duodenal ulcers in 17 patients. A significant association (P <0.001) was found between a conserved cagPAI and peptic ulcer disease (34 %). The positivity of the cagA gene varied according to the region of the gene that was amplified. The region near to the promoter was present in almost all of the H. pylori isolates (97.2 %). The segment from nt 1764 to 2083 and the extreme right end were frequently deleted in the isolates from the controls (P <0.01). The positivity of the promoter region of cagA and cagT, cagE, cagM and LEC showed a significant difference between the isolates from peptic ulcer patients and from the controls (P <0.01). Patients usually had moderate gastritis; however, the intensity of the active inflammation was higher in the peptic ulcer group (P <0.001). cagT, cagM, LEC and the right end terminus of the cagA-positive H. pylori isolates were associated with a 27-fold, 8-fold, 4-fold and 4-fold risk of peptic ulcer disease, respectively, and may be useful markers to identify individuals at higher risk of peptic ulcer disease development in Brazil.


Abbreviations: Apcag, cagA promoter region; cagPAI, cag pathogenicity island; IL, interleukin; LEC, left end of the cag II.







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 © 2007 Society for General Microbiology.