The association ofHelicobacter pylori with gastric cancer and preneoplastic gastric lesions in Chiapas, Mexico

Guarner, Jeannette; Mohar, Alejandro; Parsonnet, Julie; Halperin, David

doi:10.1002/1097-0142(19930115)71:2<297::aid-cncr2820710205>3.0.co;2-9

Cited by 91 publications

(42 citation statements)

References 14 publications

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“…They were cultured according to the instructions of the manufacturer in keratinocyte serum-free growth medium to maintain a proliferative phenotype. This medium is supplemented with 0.1 g/ml human recombinant epidermal growth factor, 5.0 mg/ml insulin, 0.5 mg/ml hydrocortisone, 50 mg/ml gentamicin, 50 g/ml amphotericin B, and 7.5 mg/ml bovine pituitary extract (BioWhittaker) at 37°C in 5% CO 2 …”

Section: Cell Linesmentioning

confidence: 56%

“…Prototypically, Helicobacter pylori has been linked to mutagenic free radical formation leading to chronic gastric inflammation and the stimulation of cellular proliferation (2)(3)(4). Mechanisms for H. pylori-induced cellular proliferation and carcinogenesis are under active investigation, but other model systems for complex interactions between bacterial pathogens and host responses, resulting in the development of cellular proliferation and the cancer phenotype are not well described.…”

mentioning

confidence: 99%

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Pseudomonas aeruginosaLipopolysaccharide Induction of Keratinocyte Proliferation, NF-κB, and Cyclin D1 Is Inhibited by Indomethacin

Preciado

Caicedo

Jhanjee

et al. 2005

The Journal of Immunology

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NF-κB is activated during acute inflammatory states as well as in other injury response disease states. Several pathologic states in squamous tissue injury response are characterized by increased squamous proliferation. This study was performed to investigate the hypothesis that Pseudomonas aeruginosa LPS is able to activate a proliferative phenotype in squamous cells via NF-κB induction and that this NF-κB-mediated response may be abrogated with the classic anti-inflammatory agent indomethacin. EMSA, luciferase reporter gene experiments, Western blots, and cellular proliferation assays were performed in normal and transformed human keratinocytes after stimulation with P. aeruginosa LPS. EMSA and luciferase reporter gene assays showed a 3- to 5-fold induction of active NF-κB in human keratinocyte cell lines after stimulation with P. aeruginosa LPS. The stimulation correlated with significantly increased cellular proliferation. As one potential mechanism for this increase in proliferation, an NF-κB-specific activation of cyclin D1 was observed. Both the NF-κB induction and proliferation response were inhibited with indomethacin and in dominant negative stable transfection clones. P. aeruginosa LPS activates proliferation of human keratinocytes, potentially through the induction of NF-κB and cyclin D1. These findings suggest that bacterial components can contribute to proliferative disease states in squamous epithelium through NF-κB activation.

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Section: Cell Linesmentioning

confidence: 56%

mentioning

confidence: 99%

Pseudomonas aeruginosaLipopolysaccharide Induction of Keratinocyte Proliferation, NF-κB, and Cyclin D1 Is Inhibited by Indomethacin

Preciado

Caicedo

Jhanjee

et al. 2005

The Journal of Immunology

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“…Although most individuals experience no symptoms, 10 to 20% develop peptic ulcer disease (25,55). Furthermore, chronic H. pylori infection confers a 3-to 12-fold increased risk of developing gastric cancers such as adenocarcinoma and low-grade B-cell lymphoma (6,23,28,41,51,52).…”

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confidence: 54%

Safety and Immunogenicity of Oral Inactivated Whole-Cell Helicobacter pylori Vaccine with Adjuvant among Volunteers with or without Subclinical Infection

et al. 2001

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Helicobacter pylori infection of the gastric mucosa can be found in approximately 50% of the world's population and is associated with a range of pathology, including peptic ulcer, atrophic gastritis, and gastric cancer. To explore immunization as a strategy for preventing and treating H. pylori-associated disease, we assessed the safety and immunogenicity in healthy adults of a formalin-inactivated, oral H. pylori whole-cell (HWC) vaccine, administered with or without mutant Escherichia coli heat-labile toxin (LT R192G ) as a mucosal adjuvant. In a dose-response study, 23 subjects with or without H. pylori infection were vaccinated with either 2.5 ؋ 10 6 HWC, 2.5 ؋ 10 8 HWC, or 2.5 ؋ 10 10 HWC, plus 25 g of LT R192G . Thereafter, a randomized study was conducted in which 18 H. pylori-infected subjects were assigned, in a double-blind fashion, to receive either 2.5 ؋ 10 10 HWC plus placebo-adjuvant, placebo-vaccine plus 25 g of LT R192G , placebo-vaccine plus placeboadjuvant, or 2.5 ؋ 10 10 HWC plus 25 g of LT R192G . Diarrhea (six subjects), low-grade fever (five subjects), and vomiting (two subjects) were observed, usually after the first dose. Significant rises in geometric mean mucosal (fecal and salivary) anti-HWC immunoglobulin A antibodies occurred among H. pylori-infected and uninfected subjects following inoculation with 2.5 ؋ 10 10 HWC plus 25 g of LT R192G . Moreover, among H. pylori-negative volunteers, this regimen induced significant lymphoproliferative responses in 5 of 10 subjects and gamma interferon production responses to H. pylori sonicate in 7 of 10 subjects. There was no evidence that vaccination eradicated H. pylori in infected volunteers. These results suggest that it is possible to stimulate mucosal and systemic immune responses in humans to H. pylori antigens by using an HWC vaccine.

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“…[1][2][3][4][5][6] This organism can be identified by culture, urea test, and histologic examination of biopsy specimens. However, these techniques were time-consuming and costly.…”

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confidence: 99%

Seroepidemiology of Helicobacter pylori infection among preschool children in Taiwan.

Lin¹,

Nieh²,

Wang³

et al. 1999

The American Journal of Tropical Medicine and Hygiene

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Abstract. Helicobacter pylori is associated with chronic antral gastritis that is related to duodenal ulcer, gastric ulcer, and probably gastric adenocarcinoma. Infection with H. pylori during childhood is considered an important risk factor for gastric carcinoma in adult life. To examine the epidemiologic characteristics of H. pylori infection among preschool children in central Taiwan, a community-based survey was carried out in 54 kindergartens in 10 urban townships, 10 metropolitan precincts, and 2 aboriginal townships randomly selected through stratified sampling. Serum specimens of 2,551 healthy preschool children (3-6 years old) randomly sampled from study kindergartens were screened for antibodies to H. pylori by latex agglutination and ELISA methods. Multivariate-adjusted odds ratios (ORs) with their 95% confidence intervals (CIs) were estimated by multiple logistic regression analysis. A total of 207 subjects were antibody-positive, giving a prevalence of 8.1%. The overall seropositive rates were 4.5% in 3-year-old group, 4.4% in 4-year-old group, 9.4% in 5-year-old group, and 11.7% in 6-year-old group. The older the age, the higher the seroprevalence (OR ϭ 3.2, 95% CI ϭ 1.5-6.8 for 3-year-old children versus the 6-year-old children). Seroprevalence was not different between boys and girls. The aboriginal townships had a seroprevalence greater than the urban townships and metropolitan precincts (OR ϭ 2.6, 95% CI ϭ 1.9-3.7). The larger the number of siblings, the higher the seroprevalence (OR ϭ 2.4, 95% CI ϭ 1.0-5.8 for those with no sibling versus those with Ն 3 siblings). In the multiple logistic regression analysis, the seroprevalence of H. pylori remained significantly increased with age, aboriginal township, and large sibship size after multivariate adjustment. A poor water supply system, sewage disposal, and other environmental hygiene in the aboriginal townships might have played some role in infection with H. pylori. The early childhood transmission among siblings might also be an important determinant of H. pylori seropositivity in Taiwan.Infection with Helicobacter pylori has been causally related to chronic gastritis and peptic ulcer, and indirectly related to gastric adenocarcinoma and primary gastric B cell lymphoma.

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The association ofHelicobacter pylori with gastric cancer and preneoplastic gastric lesions in Chiapas, Mexico

Cited by 91 publications

References 14 publications

Pseudomonas aeruginosaLipopolysaccharide Induction of Keratinocyte Proliferation, NF-κB, and Cyclin D1 Is Inhibited by Indomethacin

Pseudomonas aeruginosaLipopolysaccharide Induction of Keratinocyte Proliferation, NF-κB, and Cyclin D1 Is Inhibited by Indomethacin

Safety and Immunogenicity of Oral Inactivated Whole-Cell Helicobacter pylori Vaccine with Adjuvant among Volunteers with or without Subclinical Infection

Seroepidemiology of Helicobacter pylori infection among preschool children in Taiwan.

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