cagA and vacA status and influence of Helicobacter pylori infection on serum oxidative DNA damage in Iranian patients with peptic ulcer disease

Khodaii, Zohreh; Ghaderian, Sayyed Mohammad Hossein; Akbarzadeh, Reza; Nejati, Hadi; Panah, Akram Sadat Tabatabaei

doi:10.1007/s11845-010-0548-5

Cited by 12 publications

(7 citation statements)

References 49 publications

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“…Demirturk et al suggested that cagA positivity is associated with more severe glandular atrophy, inflammation, and activity, whereas Saruc et al demonstrated a relationship between cagA positivity with inflammation, H. pylori density, and intestinal metaplasia but not with glandular atrophy [21,22]. In our study, we found 71.2% infected patients with cagA-positive which are similar to some reports from Iran [23] and different from reports of South and East Asian where the presence of cagA strain and its association with clinical outcomes is more than 90% [24,25]. It has been shown that the prevalence of cagA-positive strains in USA and Europe is 60e70% [26].…”

Section: Discussionsupporting

confidence: 90%

Frequency of virulence factors in Helicobacter pylori-infected patients with gastritis

Salimzadeh

Bagheri

Zamanzad

et al. 2015

Microbial Pathogenesis

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Section: Discussionsupporting

confidence: 90%

Frequency of virulence factors in Helicobacter pylori-infected patients with gastritis

Salimzadeh

Bagheri

Zamanzad

et al. 2015

Microbial Pathogenesis

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“…Many other disease-associated virulence factors have now been identified, but unfortunately most seem linked to the cagA status and hence probably do not represent independent risk factors (Kusters et al, 2006). In this study, cagA was found at a similar level in all of the gastrointestinal disorders, which was somewhat unexpected considering a recent report that failed to find a significant link between cagA and H. pylori infection-associated disease types among Iranian patients (Khodaii et al, 2011). In the current study, cagA and dupA were not colinked to a specific disease type and thus they were independent predictors for the clinical outcome of H. pylori infection, as has been suggested previously Zhang et al, 2008).…”

Section: Discussionmentioning

confidence: 44%

Infection with Helicobacter pylori strains lacking dupA is associated with an increased risk of gastric ulcer and gastric cancer development

Abadi

Taghvaei

Wolfram

et al. 2012

Journal of Medical Microbiology

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Recently, dupA was reported as a new virulence factor in Helicobacter pylori, but its association with gastroduodenal disorders and its mode of action are still unclear. Here, an association of the dupA status with different disease groups was determined and a biological explanation for the observed associations was tested. In total, 216 H. pylori isolates were obtained from 232 presumed H. pylori-infected patients. A positive association was observed between the occurrence of duodenal ulcer (DU) and the presence of dupA [odds ratio (OR) 24.2; 95 % confidence interval (CI) 10.6-54.8]. In addition, an inverse association between the occurrence of gastric cancer (GC) [OR 0.16; 95 % CI 0.05-0.47] and gastric ulcer (GU) [OR 0.34; 95 % CI 0.16-0.68] with the presence of dupA was observed. A putative explanation for the observed associations might be a more corpus-located infection (pan-gastritis) by the dupA-positive strains due to their increased acid resistance. Indeed, a strong association between dupA-positive H. pylori isolated from gastritis patients and in vitro acid resistance was observed (P,0.05). The observed higher acid resistance of the dupA-positive strains suggests that these strains are adapted to a stomach with high gastric acid output. This may in part explain the observed associations, as an increased gastric acid output is thought to be typical for an antrumpredominant H. pylori infection and, whilst this is associated with an increased risk of DU formation, it also decreases the risk for the genesis of GUs and GC.

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“…Consistent with this finding, ROS and RON are important metabolites that can mediate many DNA damage signaling pathways. To this end, 8‐OH‐deoxyguanosine (8‐OHdG) and 8‐nitroguanine (8‐NG) are commonly used and are highly sensitive markers for ROS‐ and RNS‐mediated DNA oxidation, respectively . ROS and RNS can play an important role in cellular injury and carcinogenesis of gastric epithelial cells infected with H pylori .…”

Section: Overproduction Of Ros/ron: An Important Consequence Involvinmentioning

confidence: 99%

A lucid review of Helicobacter pylori‐induced DNA damage in gastric cancer

Xie

2019

Helicobacter

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Helicobacter pylori (H pylori) is the main risk factor for gastric cancer (GC). In recent years, many studies have addressed the effects of H pylori itself and of H pylori-induced chronic inflammation on DNA damage. Unrepaired or inappropriately repaired DNA damage is one possible carcinogenic mechanism. We may conclude that H pylori-induced DNA damage is one of the carcinogenic mechanisms of GC. In this review, we summarize the interactions between H pylori and DNA damage and the effects of H pylori-induced DNA damage on GC. Then, focusing on oxidative stress, we introduce the application of antioxidants in GC. At the end of this review, we discuss the outlook for further research on H pylori-induced DNA damage. K E Y W O R D SDNA damage, Helicobacter pylori, NF-κB, PLK

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cagA and vacA status and influence of Helicobacter pylori infection on serum oxidative DNA damage in Iranian patients with peptic ulcer disease

Abstract: These virulence factors are not associated with the development of PUD in Iranian patients. H. pylori infection may be associated with increased serum 8-OHdG.

Cited by 12 publications

References 49 publications

Frequency of virulence factors in Helicobacter pylori-infected patients with gastritis

Frequency of virulence factors in Helicobacter pylori-infected patients with gastritis

Infection with Helicobacter pylori strains lacking dupA is associated with an increased risk of gastric ulcer and gastric cancer development

A lucid review of Helicobacter pylori‐induced DNA damage in gastric cancer

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