The effect on serum myeloperoxidase activity and oxidative status of eradication treatment in patients Helicobacter pylori infected

doi:10.1016/j.clinbiochem.2011.03.001

Clinical Biochemistry

Volume 44, Issues 8–9, June 2011, Pages 647-649

https://doi.org/10.1016/j.clinbiochem.2011.03.001 Get rights and content

Abstract

Objectives

Myeloperoxidase activity has been investigated after eradication of Helicobacter pylori (H. pylori) in infected patients in previous studies but the results are controversial. The aim of this study was to investigate effect on serum myeloperoxidase activity and oxidative status of eradication treatment in H. pylori-infected patients.

Design and methods

Gastric biopsy specimens were obtained from 30 H. pylori infected patients. Serum myeloperoxidase activity was measured by enzyme-linked immunoassay. Oxidative status was determined using total antioxidant capacity (TAC) and total oxidant status (TOS) measurement and calculation of oxidative stress index (OSI).

Results

After 2 weeks of the eradication treatment, serum myeloperoxidase activity, TOS and OSI values were significantly lower (all; p < 0.001), while TAC was significantly higher (p < 0.001).

Conclusions

Our results indicate that eradication treatment in H. pylori-infected patients may affect both oxidative stress and myeloperoxidase activity which is an important biomarker in pathogenesis of atherosclerosis.

Introduction

Helicobacter pylori (H. pylori) is a noninvasive, microaerophile, nonspore-forming, and spiral-shaped microorganism. H. pylori causes type B chronic gastritis [1]. H. pylori is also held responsible for other nongastric diseases such as atherosclerosis, insulin resistance and diabetes mellitus [2].

H. pylori induces infiltration and activation of neutrophils and macrophages [3]. Neutrophils are considered to be major effector cells in tissue damage that occurs in inflammatory disease. Histological examination of the infected gastric mucosa shows abundant accumulation of neutrophils. Despite this and high concentrations of antibodies against H. pylori [4] the infection persists. The hallmark of chronic gastritis caused by H. pylori infection is infiltration of neutrophils into gastric mucosa [5]. Mucosal biopsy specimens from patients with H. pylori infection showed increased amounts of reactive oxygen species (ROS) and myeloperoxidase (MPO) activity [6], which may thus act as a marker for neutrophil accumulation. In addition, H. pylori density and neutrophils infiltration were correlated with MPO level in gastric mucosa [7]. MPO possesses potent proinflammatory properties and may contribute directly to tissue injury. The secretion of MPO from neutrophils can be induced directly by bacterial factors [7].

MPO is an oxidative enzyme present in phagocytes, and it is an essential part of the anti-microbial system and inflammatory regulation [8]. It is released during inflammation and may lead to irreversible protein and lipid modification, increasing levels of oxidized low density lipoprotein, and promoting atherogenesis. However, MPO also promotes oxidative damage of host tissues at sites of inflammation, including atherosclerotic lesions, [9] and is able to modify pro-atherosclerotic lipoprotein particles by its oxidative intermediates [10]. Recent investigations have suggested that MPO may be involved in the development of coronary artery disease (CAD) [11], [12].

In experimental and epidemiological studies, serum MPO activity has been investigated after eradication of H. pylori in infected subjects but the results are controversial [13], [14], [15], [16], [17], [18], [19], [20]. Furthermore, serum myeloperoxidase activity along with oxidative status have not been investigated after eradication treatment in H. pylori infected subjects. Therefore, in the present study, we aimed to investigate the effect on serum MPO activity and oxidative status of eradication treatment in H. pylori-infected patients.

Section snippets

Subjects

We studied, prospectively, 30 volunteer patients (14 males and 16 females), gastric disease and mean age of 34 ± 12 years. All the patients had been scheduled for upper digestive endoscopy because of symptoms suggestive of gastrointestinal disease.

The study protocol was carried out in accordance with the Helsinki Declaration as revised in 1989. All subjects were informed about the study protocol and written consent was obtained from each one.

Exclusion criteria

Patients were excluded if they have history of alcohol

Results

The demographic data of H. pylori-infected patients are shown in Table 1. There was no significant difference between before and after eradication treatment with respect to body mass index in H. pylori infected patients (p > 0.05).

After 2 weeks of the eradication treatment in H. pylori infected patients, serum myeloperoxidase activity, TOS level and OSI value was significantly lower (all, p < 0.001), while TAC level was significantly higher (p < 0.001) (Table 2).

Discussion

In the present study, we assayed oxidative status of the study population by using TOS and TAC along with calculation of OSI, an indicator of oxidative stress, that reflects the redox balance between oxidation and antioxidation [26]. With respect to increase in oxidative stress, our findings were in concordance with the previous studies [26], [27]. Although the concentrations of serum levels of oxidants and antioxidants can be measured individually, it may not accurately reflect the oxidative

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The effect on serum myeloperoxidase activity and oxidative status of eradication treatment in patients Helicobacter pylori infected

Abstract

Objectives

Design and methods

Results

Conclusions

Introduction

Section snippets

Subjects

Exclusion criteria

Results

Discussion

Free Radic Biol Med

J Neuroimmune

Dig Liver Dis

Clin Biochem

Clin Biochem

Cancer Lett

Clin Biochem

Am J Pathol

Helicobacter pylori: its role in disease

Clin Infect Dis

Non-gastrointestinal tract associations of Helicobacter pylori infection

Arch Intern Med

Review article: the role of inflammation in the pathogenesis of gastric cancer

Aliment Pharmacol Ther

The antibody response to Helicobacter pylori infection, and the value of serologic tests to detect H pylori and for post-treatment monitoring

Unidentified curved bacilli on gastric epithelium in active chronic gastritis

Lancet

Neutrophil degranulation by Helicobacter pylori proteins

Gut

Helicobacter pylori watersoluble surface proteins activate human neutrophils and up-regulate expression of CXC chemokines

Dig Dis Sci

Myeloperoxidase

Curr Opin Hematol

Oxidation of low-density lipoprotein with hypochlorite causes transformation of the lipoprotein into a high-uptake form for macrophages

Biochem J