H. pylori and mitochondrial changes in epithelial cells: The role of oxidative stress

Calvino-Fernández, Miryam; Parra-Cid, T.

doi:10.4321/s1130-01082010000100006

Cited by 23 publications

(10 citation statements)

References 56 publications

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“…Increasing evidence has shown that bioenergetics and mitochondrial function are impaired in FMS [42–44] and PUD [45–47] patients. Although it is unclear whether oxidative stress is a common pathway of PUD and FMS, recent studies have shown that oxidative stress can cause the pathophysiological mechanisms that culminate in the symptoms of PUD and FMS.…”

Section: Discussionmentioning

confidence: 99%

Association between fibromyalgia syndrome and peptic ulcer disease development

Wang

Lin

et al. 2017

PLoS ONE

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PurposeThe correlation of fibromyalgia syndrome (FMS) with peptic ulcer disease (PUD) is unclear. We therefore conducted a cohort study to investigate whether FMS is correlated with an increased risk of PUD.MethodsIn this study, we established an FMS cohort comprising 26068 patients aged more than 20 years who were diagnosed with FMS from 2000 to 2011. Furthermore, we established a control cohort by randomly choosing 104269 people without FMS who were matched to the FMS patients by gender, age, and index year. All patients were free of PUD at the baseline. Cox proportional hazard regressions were performed to compute the hazard ratio of PUD after adjustment for demographic characteristics and comorbidities.ResultsThe prevalence of comorbidities was significantly higher in the FMS patients than in the controls. The incidence of PUD was 29.8 and 19.4 per 1000 person-years in the FMS and control cohorts, respectively. In addition, the FMS cohort exhibited a 1.40-fold higher risk of PUD (95% confidence interval = 1.35–1.45) compared with the control cohort. After control for confounding factors, the medications (selective serotonin reuptake inhibitors, serotonin–norepinephrine reuptake inhibitors, and antidepressants) taken by the FMS patients did not increase the risk of PUD.ConclusionFMS patients exhibit a higher risk of PUD than that of patients without FMS.

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Section: Discussionmentioning

confidence: 99%

Association between fibromyalgia syndrome and peptic ulcer disease development

Wang

Lin

et al. 2017

PLoS ONE

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“…Hence, researchers have paid much attention to H. pylori. Researchers recently[4–6] found that pro- and anti-inflammatory cytokines and oxidative stress play important roles in the development of diseases such as peptic ulceration and gastric adenocarcinoma in patients with H. pylori infection. In contrast, another study regarding the effects of chronic excessive alcohol consumption on the liver and cardiovascular system has demonstrated that modest alcohol intake, such as 1–2 drinks (a standard drink is equivalent to 10 g of ethanol) per day, may decrease cardiovascular mortality[7].…”

Section: Introductionmentioning

confidence: 99%

Effect of H. pylori Infection on Cytokine Profiles and Oxidative Balance in Subjects with Chronic Alcohol Ingestion

Wang

et al. 2015

PLoS ONE

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Different amounts of ingested alcohol can have distinct effects on the human body. However, there is limited research on chronic alcohol consumption with Helicobacter pylori infection. We sought to investigate the relationship between the cytokine profile, oxidative balance and H. pylori infection in subjects with chronic alcohol consumption. A total of 142 subjects were divided into three groups: 59 subjects with chronic alcohol ingestion and H. pylori infection (group A); 53 subjects with chronic alcohol ingestion without H. pylori infection (group B); and 30 control subjects (group C). The serum levels of CagA, interleukin (IL)-10, E-selectin, TNF-α, malondialdehyde (MDA) and superoxide dismutase (SOD) activity were measured by enzyme-linked immunosorbent assay (ELISA). We found that the ages and serum H. pylori CagA levels among the three groups, as well as both the mean drinking age and the mean daily alcohol consumption between groups A and B, were matched and comparable. Comparing the BMIs among the three groups, the BMI differences were found to be statistically significant (F=3.921, P<0.05). Compared with group C, the BMIs in groups A and B were significantly higher (P<0.001 and P<0.01, respectively); however, the BMI differences between group A and group B were not statistically significant (P>0.05). Additionally, no differences in the serum CagA levels were found in comparisons among the groups (all P>0.05). The serum IL-10 and E-selectin levels in group A were significantly lower than those in group B (serum IL-10: P<0.05; E-selectin: P<0.05). The serum IL-10 in group A was significantly higher than that in group C (P<0.01); the serum E-selectin levels in group A did not significantly differ compared with those in group C (P>0.05). Furthermore, the serum IL-10 and E-selectin levels in group B were significantly higher than those in group C (serum IL-10: P<0.001; E-selectin: P<0.05); however, the serum TNF-α levels did not differ among groups (all P>0.05). Although the serum levels of MDA and SOD in groups A and B were slightly lower than those in group C, there were no significant differences among groups (all P>0.05). In conclusion, we believe that H. pylori infection might cause a significant inhibition of certain cytokine profiles in subjects with chronic alcohol ingestion. Moreover, chronically ingested alcohol may exert an adjusted inflammatory effect, but there was no association between H. pylori infection, chronic alcohol consumption and oxidative balance.

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“…In normal cells, there is a balance between apoptosis and proliferation, but in gastric disorders caused by H . pylori , this balance is altered 23 , 24 . This is of prime importance because the imbalance between apoptosis and cell proliferation determines the pathogenesis pathway of H .…”

Section: Discussionmentioning

confidence: 99%

Binding of the Helicobacter pylori OipA causes apoptosis of host cells via modulation of Bax/Bcl-2 levels

Teymournejad¹,

Mobarez²,

Hassan³

et al. 2017

Sci Rep

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The H. pylori outer inflammatory protein A (OipA) is an outer membrane protein that contributes to gastric inflammation. OipA is believed to affect intra-cellular signalling and modulate the host signalling pathways. The aim of the current study was to clarify the role of OipA in H. pylori pathogenesis and its effect on host cell signalling pathways. To this end, the oipA gene was isolated and inserted into cloning and expression vectors. The recombinant plasmid was transferred into an expression host to produce OipA, which was subsequently purified by affinity chromatography and used for antibody production. A confluent monolayer of gastric cell lines was treated with various concentrations of OipA and investigated for attachment, toxicity, and apoptosis and alterations in signalling pathways. OipA bound to gastric cell lines confirming its role in the attachment of H. pylori to host cells. The ratio of Bax/Bcl-2 and caspase3, 8, FasL in the host cells were assessed and the results showed that the Bax/Bcl-2 ratio as well as the level of cleaved-caspase 3 was elevated in OipA-treated cells. These findings suggest that OipA can bind and induce toxic events as well as triggering apoptotic cascade in host gastric cells through intrinsic pathway.

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H. pylori and mitochondrial changes in epithelial cells: The role of oxidative stress

Cited by 23 publications

References 56 publications

Association between fibromyalgia syndrome and peptic ulcer disease development

Association between fibromyalgia syndrome and peptic ulcer disease development

Effect of H. pylori Infection on Cytokine Profiles and Oxidative Balance in Subjects with Chronic Alcohol Ingestion

Binding of the Helicobacter pylori OipA causes apoptosis of host cells via modulation of Bax/Bcl-2 levels

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