Helicobacter pylori induced interleukin-8 expression in gastric epithelial cells is associated with CagA positive phenotype.

Crabtree, Jean E.; Covacci, Antonello; Farmery, Susan M.; Xiang, Zhaoying; Tompkins, David; Perry, Sharon; Lindley, I. J. D.; Rappuoli, Rino

doi:10.1136/jcp.48.1.41

Cited by 329 publications

(230 citation statements)

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“…This supports previous data that has demonstrated that CagA þ strains were associated with greater levels of DNA aneuploidy, and p53 and c-myc expression (Nardone et al, 1999). Given the possible link between H. pylori strains and chromosome 4 amplification, it is interesting to note that CagA infection has already been associated with greater IL-8 levels (Crabtree et al, 1995). It is well known that NF-kB controls IL-8 gene expression and hence CagA þ strains may induce IL-8 upregulation via an NF-kB and chromosome 4-dependent mechanism.…”

Section: Discussionsupporting

confidence: 89%

“…Helicobactor pylori strains with the CagA pathogenicity island are known to be more virulent, producing more severe pathological infection in humans (Blaser, 1998). CagA þ strains are highly immunogenic strains of H. pylori and are associated with increased cytokine expression (Crabtree et al, 1995), inflammatory cell infiltrate and release of ROS adjacent to gastric mucosa (Fiocca et al, 1994;Sipponen et al, 1998). The oxidative DNA damage induced by ROS is an important mechanism in carcinogenesis.…”

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confidence: 99%

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Fluorescence in situ hybridisation analysis of chromosomal aberrations in gastric tissue: the potential involvement of Helicobacter pylori

et al. 2005

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In this series of experiments, a novel protocol was developed whereby gastric cells were collected using endoscopic cytology brush techniques, and prepared, such that interphase fluorescence in situ hybridization (FISH) could be performed. In total, 80 distinct histological samples from 37 patients were studied using four chromosome probes (over 32 000 cells analysed). Studies have previously identified abnormalities of these four chromosomes in upper GI tumours. Using premalignant tissues, we aimed to determine how early in Correa's pathway to gastric cancer these chromosome abnormalities occurred. Aneuploidy of chromosomes 4, 8, 20 and 17(p53) was detected in histologically normal gastric mucosa, as well as in gastritis, intestinal metaplasia, dysplasia and cancer samples. The levels of aneuploidy increased as disease severity increased. Amplification of chromosome 4 and chromosome 20, and deletion of chromosome 17(p53) were the more common findings. Hence, a role for these abnormalities may exist in the initiation of, and the progression to, gastric cancer. Helicobactor pylori infection was determined in premalignant tissue using histological analysis and PCR technology. Detection rates were comparable. PCR was used to subtype H. pylori for CagA status. The amplification of chromosome 4 in gastric tissue was significantly more prevalent in H. pylori-positive patients (n ¼ 7) compared to H. pylori-negative patients (n ¼ 11), possibly reflecting a role for chromosome 4 amplification in H. pylori-induced gastric cancer. The more virulent CagA strain of H. pylori was associated with increased disease pathology and chromosomal abnormalities, although numbers were small (CagA þ n ¼ 3, CagAÀ n ¼ 4). Finally, in vitro work demonstrated that the aneuploidy induced in a human cell line after exposure to the reactive oxygen species (ROS) hydrogen peroxide was similar to that already shown in the gastric cancer pathway, and may further strengthen the hypothesis that H. pylori causes gastric cancer progression via an ROS-mediated mechanism.

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Section: Discussionsupporting

confidence: 89%

mentioning

confidence: 99%

Fluorescence in situ hybridisation analysis of chromosomal aberrations in gastric tissue: the potential involvement of Helicobacter pylori

et al. 2005

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“…Crabtree et al 9 and Peek et al 10 reported that H. pylori strains with the cagA gene induce high IL-8 production and in strains without this gene produce less IL-8. However, while high neutrophil in®ltration was observed in the antrum of duodenal ulcer patients with H. pylori antral + body infection, hardly any neutrophil in®ltration was noted in the body of the stomach.…”

Section: Discussionmentioning

confidence: 99%

Gastric corpus IL‐8 concentration and neutrophil infiltration in duodenal ulcer patients

Uemura

Oomoto

Mukai

et al. 1997

Aliment Pharmacol Ther

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Background: The purpose of the present study was to examine the association between interleukin‐8 (IL‐8) in the gastric body due to Helicobacter pylori infection and histological gastritis, as well as elucidating the effect of acid secretion inhibitors on H. pylori associated body gastritis in duodenal ulcer patients. Methods: Twenty H. pylori‐negative patients, 20 H. pylori‐positive patients with chronic gastritis without peptic ulceration, and 20 H. pylori‐positive duodenal ulcer patients (DU) were studied. Four biopsy samples were taken, each from the greater curvature of the antrum and body of the stomach. Biopsies were histologically investigated by ELISA to determine the density of H. pylori, the degree of neutrophil infiltration and the IL‐8 concentration in the mucosa. Results: In the gastric mucosa of H. pylori‐negative subjects, no IL‐8 and hardly any neutrophil infiltration were observed. In contrast, enhanced IL‐8 production and increased neutrophil infiltration were present in those infected with H. pylori. In H. pylori‐positive patients, a significant correlation was observed between the IL‐8 concentration and the degree of neutrophil infiltration, but no correlation was found in the body mucosa of those with DU. Twelve of 20 DU patients demonstrated hardly any neutrophil infiltration, despite the increased mucosal IL‐8 content in the body. The administration of omeprazole in DU patients markedly increased mucosal neutrophil infiltration even though it did not cause any significant change in the H. pylori density and IL‐8 concentration in the body. Although the effect of omeprazole was transient, a significant increase in neutrophil infiltration continued in comparison with the status before omeprazole administration in those subsequently undergoing maintenance treatment with H2‐blockers. Conclusion: In H. pylori‐positive chronic gastritis, IL‐8 concentration is enhanced in the mucosa of the body, and is associated with increased neutrophil infiltration. However, in DU patients, despite increases in body IL‐8 concentration, neutrophil infiltration is reduced and the gastritis may be localized in the antrum.

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“…77,97,98 In addition, only type I strains were able to elicit secretion of Interleukin 8 (IL-8), which is the mediator of neutrophil migration by epithelial cells in vitro. 99,100 A number of epidemiological studies have shown that there is a strong correlation between infection with type I strains and occurrence of severe gastroduodenal diseases, whereas type II strains with attenuated virulence do not induce dramatic change in the gastric mucosa. 97,101 Thus, H. pylori strains that express CagA cause more extensive inflammation of the gastric mucosa, 99,100,102 and infections with these strains have been reported to be more likely to result in peptic ulceration, 97,98 atrophic gastritis 101 and gastric adenocarcinoma.…”

Section: Relevance Of Strain Types Of H Pylori In the Outcome Of Infmentioning

confidence: 99%

Helicobacter pylori: recent advances in the study of its pathogenicity and prevention

Aguilar¹,

Ayala²,

Fierros-Zarate³

2001

Salud pública Méx

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Helicobacter pylori has acquired great importance during the last two decades, after being recognized as an important pathogen that infects a great portion of the human population. This microorganism is recognized as the main causal agent of chronic gastritis and duodenal ulcers, and it is associated with the subsequent development of gastric carcinoma. The pathogenic mechanisms of H. pylori and their relation to gastric ailments have not been clearly defined. However, at present it is well established that urease, vacuolating cytotoxin VacA, and the pathogenicity island (cag PAI) gene products, are the main factors of virulence of this organism. Thus, individuals infected with strains that express these virulence factors probably develop a severe local inflammation that may induce the development of peptic ulcer and gastric cancer. The way the infection spreads throughout the world suggests the possibility that there are multiple pathways of transmission. Due to the importance that H. pylori has acquired as a human pathogen, laboratories worldwide are attempting to develop a vaccine that confers long-term immunological protection against infection by this microorganism. Hence, the objective of this review is to present the most relevant findings of the biology of H. Pylori and its interaction with the human host. The full version of this paper is available too at: http:// www.insp.mx/salud/index.html ResumenHelicobacter pylori ha adquirido gran importancia durante las últimas dos décadas, al ser reconocido como un importante patógeno que infecta una gran porción de la población humana. Este microrganismo es reconocido como el principal agente que causa la gastritis crónica y la úlcera duodenal, además de que se ha asociado con el subsecuente desarrollo del carcinoma gástrico. Los mecanismos patogé-nicos de H. pylori y su relación con los padecimientos gás-tricos no se han definido en forma clara. Sin embargo, actualmente está bien establecido que la ureasa, la citotoxina vacuolizante VacA y los productos de los genes de la isla de patogenicidad (cag PAI) son los principales factores de virulencia de este organismo. Así, los individuos infectados con cepas que expresan dichos factores de virulencia, probablemente manifiesten una marcada inflamación local que podría inducir el desarrollo de úlcera péptica y cáncer gástri-co. La manera como la infección se propaga a nivel mundial sugiere la posibilidad de múltiples vías de transmisión. A consecuencia de la importancia que H. pylori ha adquirido como patógeno humano, los laboratorios del mundo se esfuerzan para desarrollar una vacuna que confiera protección inmunológica de larga duración contra la infección por este microorganismo. El objetivo de esta revisión es presentar los hallazgos más relevantes sobre la biología de H. pylori y su interacción con su huésped humano. El texto completo de este artículo también está disponible en:

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Helicobacter pylori induced interleukin-8 expression in gastric epithelial cells is associated with CagA positive phenotype.

Abstract: (7 Clin Pathol 1995;48:41-45)

Cited by 329 publications

References 32 publications

Fluorescence in situ hybridisation analysis of chromosomal aberrations in gastric tissue: the potential involvement of Helicobacter pylori

Fluorescence in situ hybridisation analysis of chromosomal aberrations in gastric tissue: the potential involvement of Helicobacter pylori

Gastric corpus IL‐8 concentration and neutrophil infiltration in duodenal ulcer patients

Helicobacter pylori: recent advances in the study of its pathogenicity and prevention

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