DNA damage and repair in Helicobacter pylori-infected gastric mucosa cells

Arabski, Michał; Klupińska, Grażyna; Chojnacki, Jan; Kaźmierczak, Paweł; Wiśniewska-Jarosińska, Maria; Drzewoski, Józef; Błasiak, Janusz

doi:10.1016/j.mrfmmm.2004.10.006

Cited by 38 publications

(24 citation statements)

References 16 publications

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“…The development of gastric cancer associated with the H. pylori infection is predominantly a result of the immune responses of gastric epithelial cells. Nevertheless, the process of carcinogenesis involves genetic alterations, consequently there may be a link between H. pylori infection and DNA of host cells [25]. One of the factors contributing to this phenomenon could be the patchy density of H. pylori that could be associated with chronic inflammation and activity [26].…”

Section: Discussionmentioning

confidence: 99%

Relationship among Oxidative DNA Damage, Gastric Mucosal Density and the Relevance of cagA, vacA and iceA Genotypes of Helicobacter pylori

et al. 2007

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The aim of this study was to evaluate the relationship among oxidative DNA damage, density of Helicobacter pylori and the relevance of cagA, vacA and iceA genotypes of H. pylori. Gastric epithelial cells were isolated from 24 uninfected patients, 42 H. pylori infected patients with gastritis, and 61 patients with gastric cancer. Oxidative DNA damage was analyzed by the Comet assay, the density of H. pylori was measured by real-time polymerase chain reaction (PCR), and allelic variants of cagA, vacA and iceA were identified using the PCR. Infected patients by Helicobacter pylori cagA(+), vacAs1 m1 and iceA1 genotype showed higher levels of oxidative DNA damage than infected patients with H. pylori cagA(-), vacAs2 m2 and iceA2 genotypes and uninfected patients. Density of H. pylori did not influence oxidative DNA damage. Our results indicate that H. pylori genotype is more relevant than density for oxidative DNA damage.

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Section: Discussionmentioning

confidence: 99%

Relationship among Oxidative DNA Damage, Gastric Mucosal Density and the Relevance of cagA, vacA and iceA Genotypes of Helicobacter pylori

et al. 2007

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“…57,141,142 Most isolates of C jejuni produce a toxin called CdtB (cytolethal distending toxin B) that causes direct DNA damage. 143 CdtB induces double-strand DNA breaks and growth arrest in T lymphocytes and may thus participate in immune evasion mechanisms during infection with CdtB-producing bacteria, 143 as well as the emergence of the DNA breaks in B cells leading to the synthesis of a truncated immunoglobulin as seen in IPSID patients.…”

Section: Ongoing Mutations In Proliferating Lymphocytesmentioning

confidence: 99%

Infection-associated lymphomas derived from marginal zone B cells: a model of antigen-driven lymphoproliferation

Suarez

2006

Blood

399

296

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IntroductionThe geographic heterogeneity in the incidence of B-cell nonHodgkin lymphomas (NHLs) suggests that environmental factors such as infections might have a role in lymphomagenesis. 1,2 Because of the inherent genetic instability of lymphocytes, lymphoid proliferation increases the risk of transformation, and sustained activation of the lymphoid system, which can be observed during chronic infection, immunodeficiency, and autoimmunity, constitutes a risk factor for lymphomas. [3][4][5] Congenital and acquired immunodeficiencies associated with HIV infection and solid organ or hematopoietic transplantation increase the risk of developing B-cell NHLs. 6,7 Similarly, Sjögren syndrome and other autoimmune conditions are also associated with an increased risk of lymphomas. 8,9 Certain types of lymphomas are associated with specific microbial infections, and infection-associated lymphomas currently fall in diverse histopathologic categories (Table 1). 10 Infections may contribute to lymphomagenesis by promoting favorable conditions for lymphocyte transformation, such a increased proliferation or decreased apoptosis of lymphoid cells. 11 Direct lymphocyte transformation by a given microbial agent is the simplest scenario accounting for infection-associated lymphomas. Lymphotropic transforming viruses such as Epstein-Barr virus (EBV), human herpesvirus 8 (HHV8), and human Tlymphotropic virus 1 (HTLV-1) directly infect a subset of lymphoid cells in which they express viral oncogenes. [12][13][14] An alternative scenario to direct transformation of lymphocytes has more recently emerged for microbial species associated with lymphomas but that do not directly infect or transform lymphoid cells. They have in common the ability to persist chronically in host tissues and trigger a sustained lymphoid proliferation, giving a selective advantage to lymphoid clones that still remain dependent upon antigen stimulation. 15,16 According to this model, the microbial pathogen is neither intrinsically transforming nor oncogenic, but can be viewed as a chronic source of antigens increasing the proliferative rate of lymphoid effectors, hence fueling the transformation process. This model has emerged with the description of several lymphomas developing in the context of chronic antigen-dependent immune stimulation, among which H pylori-associated gastric mucosa-associated lymphoid tissue (MALT) lymphoma is the best characterized 15,17,18 (Figure 1). Precise elucidation of the mechanisms underlying this "indirect" lymphomagenesis as well as completion of the inventory of the microbial species driving these antigen-dependent lymphoproliferations may provide important clues for their early diagnosis and the rationalization of the therapeutic interventions for this subtype of lymphomas.This group of lymphomas often involves extranodal sitesnormally devoid of organized lymphoid tissue-and manifests initially as indolent low-grade proliferations, reminiscent of the normal lymphoid hyperplasia driven by a physiologic antigenic stimulation....

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“…[9] with some modifications as described previously [11]. The objects were observed at 200× magnification with an Eclipse fluorescence microscope (Nikon, Tokyo, Japan) attached to a COHU 4910 video camera (Cohu, San Diego, CA, USA) equipped with a UV-1 filter block (an excitation filter of 359 nm and a barrier filter of 461 nm) and connected to a personal computer-based Lucia-Comet v. 4.51 image analysis system (Laboratory Imaging, Prague, Czech Republic).…”

Section: Comet Assaymentioning

confidence: 99%

“…MNNG is one of the most powerful mutagens -it methylates oxygen and nitrogen atoms in DNA via the SN 1 mechanism, in which there is a loss of the leaving group and the generation of a carbocation intermediate with the rapid attack of a nucleophile on the electrophilic carbocation to form a new σ bond [10]. We previously showed that reactive oxygen and nitrogen species generated by inflammatory cells in response to H. pylori infection may damage the DNA in GMCs, producing oxidized DNA bases and strand breaks [11]. In this study, we evaluated the reaction of the H. pylori-infected and non-infected GMCs and PBLs to MNNG in terms of DNA damage and repair.…”

Section: Introductionmentioning

confidence: 99%

Helicobacter pylori infection can modulate the susceptibility of gastric mucosa cells to MNNG

Arabski

Kaźmierczak²,

Wiśniewska-Jarosińska

et al. 2006

Cellular and Molecular Biology Letters

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Abstract:The pathogenesis of stomach cells can be associated with their susceptibility to exogenous dietary irritants, like nitrosamines such as dimethylnitrosamines (DMNA), and to the effects of non-dietary factors, including Helicobacter pylori infection. We used N-methyl-N'-nitro N-nitrosoguanidyne (MNNG) as a surrogate agent that induces a spectrum of DNA damage similar to DMNA. Using the alkaline comet assay, we showed that antioxidants -vitamins C and E, quercetin, and melatonin -reduced the genotoxic effect of MNNG in H. pylori-infected and non-infected human gastric mucosa cells (GMCs). To compare the sensitivity of the stomach and the blood, the experiment was also carried out in peripheral blood. We observed a higher level of DNA damage induced by MNNG in H. pylori-infected than in noninfected GMCs. We did not note any difference in the efficacy of the repair of the damage in either type of GMC.

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DNA damage and repair in Helicobacter pylori-infected gastric mucosa cells

Cited by 38 publications

References 16 publications

Relationship among Oxidative DNA Damage, Gastric Mucosal Density and the Relevance of cagA, vacA and iceA Genotypes of Helicobacter pylori

Relationship among Oxidative DNA Damage, Gastric Mucosal Density and the Relevance of cagA, vacA and iceA Genotypes of Helicobacter pylori

Infection-associated lymphomas derived from marginal zone B cells: a model of antigen-driven lymphoproliferation

Helicobacter pylori infection can modulate the susceptibility of gastric mucosa cells to MNNG

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