Implication of the Structure of the<i>Helicobacter pylori cag</i>Pathogenicity Island in Induction of Interleukin-8 Secretion

Audibert, Céline; Burucoa, Christophe; Janvier, Blandine; Fauchère, Jean-Louis

doi:10.1128/iai.69.3.1625-1629.2001

Cited by 59 publications

(49 citation statements)

References 28 publications

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“…Fifty per cent of strains from West India are devoid of the entire island of genes (Kauser et al, 2004), 32 % in France (Audibert et al, 2001), 9 % in Sweden (Nilsson et al, 2003) and the USA (Hsu et al, 2002) and 1 % in Japan (Ikenoue et al, 2001). In the present report, none of the strains showed complete deletion of the cagPAI genes.…”

Section: Amplification Of Cagpai Genesmentioning

confidence: 54%

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

Mattar

Marques

Monteiro

et al. 2007

Journal of Medical Microbiology

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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. INTRODUCTIONHelicobacter pylori colonizes the human stomach causing chronic gastritis. A small number of individuals progress to peptic ulcer or gastric cancer. Multiple bacterial and/or host factors are involved in disease development (Backert et al., 2004;Peek, 2005).H. pylori clinical isolates are classified into two types according to their degree of pathogenicity. Type I, associated with severe disease pathology, expresses functional VacA (vacuolating cytotoxin A) and contains an insertion of 40 kb of foreign DNA, the cag (cytotoxin-associated gene) pathogenicity island (cagPAI). Type II lacks cagPAI, harbours a non-toxic form of VacA and is regarded as less virulent (Censini et al., 1996;Backert et al., 2004).The cagPAI may be divided into two regions, cag I and cag II, by a novel insertion sequence (IS605). There are approximately 16 and 15 open reading frames in cag I and cag II, respectively (Censini et al., 1996; Akopyants et al., 1998). The cagPAI encodes a type IV secretion system, which delivers CagA into the cytosol of gastric epithelial cells (Covacci & Rappuoli, 2000) through a rigid needle structure covered by Cag7 or CagY, a VirB10-homologous protein, and CagT, a VirB7-homologous protein, at the base (Rohde et al., 2003). CagA is tyrosine-phosphorylated by Src-family kinases (Selbach et al., 2002), triggering the elongated hummingbird phenotype (Higashi et al., 2005) similar to that of hepatocyte growth factor (Segal et al., 1999). Numerous phosp...

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Section: Amplification Of Cagpai Genesmentioning

confidence: 54%

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

Mattar

Marques

Monteiro

et al. 2007

Journal of Medical Microbiology

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“…Correlation between integrity of cagPAI, types of EPIYA motifs, and disease outcome was confirmed by several studies (24,(38)(39)(40)(41)(42). However, there are studies that reported contrary results (43)(44)(45). Variation in H. pylori genome from various areas and presence of polymorphisms in different gene loci of cagPAI could be main causes of the differences among the studies.…”

Section: Discussionmentioning

confidence: 76%

Functional Cytotoxin Associated Gene A in Helicobacter pylori Strains and Its Association with Integrity of Cag-pathogenicity Island and Histopathological Changes of Gastric Tissue

Fazeli

Alebouyeh

Tavirani

et al. 2017

Arch Clin Infect Dis

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Objectives: Existence of cytotoxin associated gene A (cagA) is considered as a marker for detection of an oncogenic Helicobacter pylori strain. Expression of cagA in the strains with incomplete delivery system (partial CagPAI) could convert them to less virulent strains.This study was aimed to analyze expression of cagA in H. pylori strains presenting diverse cagPAI and its effect on histopathological changes of the gastric tissue. Methods: Clinical strains of H. pylori and related histopathological data were obtained to examine the presence of 12 cagPAI segments by PCR. Expression of cagA was analyzed by RT-PCR as well as Immunoblotting on RNA and protein extracts of the cagPAIpositive strains, respectively. In situe expression of CagA-positive strains was determined in a gastric epithelial cell line. Results: Intact cagPAI was detected among 33% (4/12) of H. pylori strains. Out of 7 diverse cagPAI genotypes in these strains, expression of cagA was confirmed in 2 strains with complete cagPAI at both RNA and protein levels. Occurrence of intestinal metaplasia and severe active gastritis were mainly detected in the strains with complete cagPAI genotype. No association was detected between EPIYA types of the strains and expression of cagA. Conclusions: These results collectively showed high diversity of cagA and cagPAI among the H. pylori strains. These diversities may provide some reasons to explain distinct disease severity caused by different H. pylori strains in the gastric tissue.

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“…H. pylori microevolution can determine loss of all or part of the cagPAI [23]. In Japanese and French studies, cagE was found to be a better marker for the presence of cagPAI than cagA [36,37]. We did not perform detection of cagPAI empty site, and this is a limitation of our work.…”

Section: Discussionmentioning

confidence: 89%

Correlation of Helicobacter pylori Genotypes with Gastric Histopathology in the Central Region of a South-European Country

et al. 2014

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Background Outcome of Helicobacter pylori (H. pylori) infection results from interaction of multiple variables including host, environmental and bacterial-associated virulence factors. Aim This study aimed to investigate the correlation of cagA, cagE, vacA, iceA and babA2 genotypes with gastric histopathology and disease phenotype in the central region of a South-European country. Methods This prospective study involved 148 infected patients (110 female; mean age 43.5 ± 13.4 years) submitted to endoscopy with corpus and antrum biopsies. H. pylori was cultured and DNA extracted from the isolates. Genotypes were determined by PCR. Histopathological features were graded according to the updated Sydney system and OLGA/OLGIM classification. Only patients with single H. pylori genotypes and complete histopathological results were included.Results Antrum samples presented higher degrees of atrophy, intestinal metaplasia, chronic inflammation and neutrophil activity. Genotype distribution was as follows: cagA-31.8 %; cagE-45.9 %; vacA s1a-24.3 %; vacA s1b-19.6 %; vacA s1c-0.7 %; vacA s2-55.4 %; vacA m1-20.9 %; vacA m2-79.1 %; vacA s1m1-18.9 %; vacA s1m2-25.7 %; vacA s2m1-2 %; vacA s2m2-53.4 %; iceA1-33.8 %; iceA2-66.2 %; babA2-12.2 %. CagA genotype was significantly associated with higher degrees of intestinal metaplasia, neutrophil activity, chronic inflammation and OLGIM stages. BabA2 was linked with higher H. pylori density. Strains with vacA s1m1 or vacA s1m1 ? cagA positive genotypes had a significant association with peptic ulcer and vacA s2m2 with iron-deficient anemia. Conclusions cagA, vacA s1m1 and babA2 genotypes are relatively rare in the central region of Portugal. cagApositive strains are correlated with more severe histopathological modifications. This gene is commonly associated

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Implication of the Structure of theHelicobacter pylori cagPathogenicity Island in Induction of Interleukin-8 Secretion

Cited by 59 publications

References 28 publications

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

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

Functional Cytotoxin Associated Gene A in Helicobacter pylori Strains and Its Association with Integrity of Cag-pathogenicity Island and Histopathological Changes of Gastric Tissue

Correlation of Helicobacter pylori Genotypes with Gastric Histopathology in the Central Region of a South-European Country

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