Abstract

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.

Highlights

  • Helicobacter pylori (H. pylori) has been recognized as a class I carcinogen by the International Agency for Research on Cancer[1]

  • Another comparative study[2] showed that induced H. pylori-related TNFα is concentrated in the gastric mucosa; this pathogen does not cause any significant changes in the gastric mucosa level of IL-10 and the serum levels of TNF-α and IL-10

  • High IL-10 expression may indicate that regulatory T cells play a role in the chronic phase of H. pylori infection[17]

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Summary

Introduction

Helicobacter pylori (H. pylori) has been recognized as a class I carcinogen by the International Agency for Research on Cancer[1]. Numerous studies have demonstrated that H. pylori infection and alcohol abuse play a role in the pathogenesis of a wide variety of gastrointestinal tract conditions and diseases, including a variety of cancers, and extra-digestive conditions and diseases. Researchers recently[4,5,6] 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. A study showed that cytokines are produced by many cells, and they play the role of mediators in the development of local and systemic inflammatory reactions[11]. The aims of this study were to evaluate the associations between chronic alcohol ingestion with H. pylori infection and inflammation or lipid peroxidation by measuring the serum levels of inflammatory cytokines, anti-inflammatory cytokines, oxidative stress and antioxidants

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