Gastric Epithelial Expression of Macrophage Migration Inhibitory Factor is not Altered by <i>Helicobacter pylori</i> Infection in Humans

Lebiedz, Pia; Heidemann, Jan; Lügering, Andreas; Riedel, Susanne; Herbst, Hermann; Domschke, Wolfram; Kucharzik, Torsten

doi:10.1111/j.1523-5378.2006.00411.x

Cited by 6 publications

(5 citation statements)

References 30 publications

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“…The effect was blocked with anti-MIF antibody, suggesting the role of MIF as a mediator of H . pylori -induced tumorigenesis [34–37]. The progressive increase of epithelial and serum MIF levels in H .…”

Section: Discussionmentioning

confidence: 99%

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Correlation between macrophage migration inhibitory factor and autophagy in Helicobacter pylori-associated gastric carcinogenesis

et al. 2019

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The role of macrophage migration inhibitory factor (MIF) and autophagy in gastric cancer is not clear. We determined H. pylori infection status of the subjects and investigated the expression of MIF and autophagy markers (Atg5, LC3A and LC3B) in human gastric tissue at baseline. Then H. pylori eradication was done for H. pylori positive patients and MIF and Atg5 levels were investigated on each follow-up for both H. pylori-eradicated and H. pylori negative patients. Baseline tissue mRNA expression of MIF, Atg5, LC3A and LC3B was measured by real-time PCR in 453 patients (control 165, gastric dysplasia 82, and gastric cancer 206). Three hundred three patients (66.9%) had H. pylori infection at the time of enrollment. Only within H. pylori-positive group, MIF level was significantly elevated in patients with cancer than in control or dysplasia groups (P<0.05). LC3A and LC3B levels also showed significant differences within H. pylori-positive subgroups. H. pylori-positive dysplasia subgroup showed significantly lower (LC3A) (P<0.05) and higher (LC3B) mRNA levels (P<0.05) than in other subgroups. On follow-up, within H. pylori-eradicated group, Atg5 expression increased sequentially from control to dysplasia and cancer subgroups. Multiple linear regression showed autophagy markers (LC3A, LC3B, and Atg5) directly predicted MIF level (adjusted R2 = 0.492, P<0.001). Serial follow-up showed longitudinal increase in Atg5 level in general, with constantly higher levels in H. pylori-eradicated group than in -negative group. Intestinal metaplasia (IM) group initially showed higher Atg5 expression than the IM-negative group. However, it was reversed between the groups eventually because of the lower rate of increase in IM group. These results suggest a role of MIF and autophagy markers and their interaction in H. pylori-associated gastric carcinogenesis.

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Section: Discussionmentioning

confidence: 99%

“…However, another report suggested that MIF expression and secretion did not directly increase after H . pylori infection, although IL-8 expression and secretion were upregulated [37].…”

Section: Discussionmentioning

confidence: 99%

Correlation between macrophage migration inhibitory factor and autophagy in Helicobacter pylori-associated gastric carcinogenesis

et al. 2019

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“…Although H. pylori infection has been reported to increase serum MIF (Xia et al , 2005), other reports have shown little effect of H. pylori on circulating levels of MIF (He et al , 2006; Mohri et al , 2009) and H. pylori infection does not increase expression of MIF in gastric epithelium (Lebiedz et al , 2006). In our study, H. pylori infection appears not to be a contributory factor in raising MIF serum levels (Figure 2).…”

Section: Discussionmentioning

confidence: 99%

Macrophage migration inhibitory factor and DJ-1 in gastric cancer: differences between high-incidence and low-incidence areas

et al. 2012

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Background:There is a need for sensitive and specific blood-borne markers for the detection of gastric cancer. Raised serum macrophage inhibitory factor (MIF) levels have been proposed as a marker for gastric cancer diagnosis but, to date, studies have only encompassed patients from high-incidence areas.Methods:We have compared the serum concentration of MIF in a large cohort of UK and Japanese gastric cancer patients, together with appropriate control subjects (age and gender matched). Carcinoembryonic antigen and H. pylori IgG were also measured, as was DJ-1, a novel candidate protein biomarker identified by analysis of gastric cancer cell line secretomes.Results:Marked elevations of the serum concentration of MIF and DJ-1 were seen in Japanese patients with gastric cancer compared with Japanese controls, a trend not seen in the UK cohort. These results could not be accounted for by differences in age, disease stage or H. pylori status.Conclusion:In regions of high, but not low incidence of gastric cancer, both MIF and DJ-1 have elevated serum concentrations in gastric cancer patients, compared with controls. This suggests that differing mechanisms of disease pathogenesis may be at play in high- and low-incidence regions.

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“…Xia et al (2005) showed that Hp might stimulate MIF expression, further promoting the proliferation of gastric epithelial cells. However, Lebiedz et al (2006) showed that MIF expression was not related to gastritis mucosa Hp infection and concluded that it had yet to be determined whether Hp infection would stimulate MIF expression and promote gastric mucosal inflammation. Nishihira (2012) suggested that MIF played a significant role in disease and that MIF knockdown could significantly decrease the pathological damage in inflammatory bowel disease.…”

Section: Discussionmentioning

confidence: 99%

Expression of macrophage migration-inhibitory factor in duodenal ulcer and its relation to Helicobacter pylori infection

Yu¹,

Zhang²,

Yang³

et al. 2015

Genet. Mol. Res.

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ABSTRACT. The aim of this study was to examine the expression of macrophage migration-inhibitory factor (MIF) in duodenal ulcer epithelial cells and its relation to Helicobacter pylori (Hp) infection, and to discuss the pathogenic roles of MIF expression and Hp infection in duodenal ulcer. MIF protein and mRNA expression was examined in samples from patients with duodenal ulcer with and without Hp infection (N = 40 each, experimental group), and in normal duodenal bulb mucosal tissue (N = 40, control group) using immunohistochemistry and in situ hybridization. Patients without Hp infection received routine treatment, and treatment was provided to the patients positive for Hp to eradicate Hp infection. Hp and MIF expression levels before treatment and after the ulcer had been cured were compared. The positive rates of MIF protein and mRNA in patients with Hp infection before treatment were 67.5 and 65%, respectively, and were 18.9 and 21.6% in the 37 patients from whom Hp was eliminated. These were statistically different both before and after treatment compared with controls (P < 0.05). In the patients without Hp infection, the positive rates of MIF protein and Macrophage MIF expression and H. pylori in duodenal ulcer mRNA expression before (45 and 47.5%, respectively) and after (32.5 and 30%) treatment were not significantly different (P > 0.05). The results of this study suggested that MIF is related to the development of duodenal ulcer, and that the presence of Hp is closely related with the expression of MIF in the duodenal mucosa and the development of duodenal ulcer.

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Gastric Epithelial Expression of Macrophage Migration Inhibitory Factor is not Altered by Helicobacter pylori Infection in Humans

Cited by 6 publications

References 30 publications

Correlation between macrophage migration inhibitory factor and autophagy in Helicobacter pylori-associated gastric carcinogenesis

Correlation between macrophage migration inhibitory factor and autophagy in Helicobacter pylori-associated gastric carcinogenesis

Macrophage migration inhibitory factor and DJ-1 in gastric cancer: differences between high-incidence and low-incidence areas

Expression of macrophage migration-inhibitory factor in duodenal ulcer and its relation to Helicobacter pylori infection

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