Increased gastric production of interleukin-8 and tumour necrosis factor in patients with Helicobacter pylori infection.

Fan, Xue‐Gong; Chua, Andrew Seng Boon; Fan, X. J.; Keeling, P. W. N.

doi:10.1136/jcp.48.2.133

Cited by 139 publications

(105 citation statements)

References 20 publications

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“…In a study on circulating serum levels of IL-6, IL-8 and TNF-α in patients with H. pylori infection, there was not a significant difference in serum levels of TNF-α and age and gender between positive and negative H. Pylori groups (23), which is consistent with the results of our study. The results of this study and the study by Fan showed that the pathogen makes no significant change in serum levels of TNF-α (23,24). However, data from our study showed an increase in serum levels of IL-1β and TNF-α cytokines in people infected with H. pylori, in another study, the average of these two cytokines was significantly higher in infected group with H. pylori than non-infected individuals (22,25).…”

Section: Discussioncontrasting

confidence: 47%

Correlation of 16s rRNA with serum levels of the cytokines, TNF-α and IL-1β, in subjects with a positive Helicobacter pylori Stool Antigen test (HPSA)

Moradipour

Khosravi

Mehrabi

et al. 2016

JBRMS

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Introduction:Helicobacter pylori (H. pylori), is a bacterium responsible for upper gastrointestinal tract diseases. The 16s rRNA is a common H. pylori gene which are usually preferred for diagnosis purpose. The aim of this study was to determine the prevalence and abundance of 16s rRNA in fecal samples and also evaluate correlation between the level of 16s rRNA and activities of the cytokines, TNF-α and IL-1β, in serum. Materials and methods:The present study was performed on 84 subjects with digestion problems. Fecal and blood samples were collected and 16s rRNA gene was assayed using PCR. The serum levels of TNF-α and IL-1β levels were measured by enzyme-linked immunosorbent assay (ELISA). Results:The results of the study revealed that there was a positive correlation between the 16s rRNA gene, H. pylori stool antigen (HPSA) and TNF-α cytokine. The study also noted that with every unit of increase in either of the quantified parameters of HPSA and IL-1β, the presence of 16s rRNA in fecal samples, showed a 2.98 and 1.01 times rise, respectively. Conclusion: According to the obtained results, it may be concluded that activities of cytokine TNF-a correlated well with the presence of HPSA and 16srRNA gene in the stomach's lining. Increase in the activities of HPSA and TNF-a cytokine could be associated with the presence of 16s rRNA in feces.

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Section: Discussioncontrasting

confidence: 47%

Correlation of 16s rRNA with serum levels of the cytokines, TNF-α and IL-1β, in subjects with a positive Helicobacter pylori Stool Antigen test (HPSA)

Moradipour

Khosravi

Mehrabi

et al. 2016

JBRMS

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“…7 Among these chemokines, interleukin-8 (IL-8), a prototype CXC chemokine, seems to play an important role in recruiting and activating neutrophils in the gastric mucosa. 8 Several reports suggest that gastric epithelial cells represent an important source of IL-8. 8,9 In addition to chemotactic potential, IL-8 is capable of activating polymorphonuclear leukocyte degranulation, the respiratory burst, and the 5-lipoxygenase pathway.…”

mentioning

confidence: 99%

“…8 Several reports suggest that gastric epithelial cells represent an important source of IL-8. 8,9 In addition to chemotactic potential, IL-8 is capable of activating polymorphonuclear leukocyte degranulation, the respiratory burst, and the 5-lipoxygenase pathway. 6 Thus, IL-8 may be a component of the inflammatory cascade.…”

mentioning

confidence: 99%

“…Indeed, gastric mucosal levels of IL-8 correlates with histological severity in patients with H. pylori-induced gastritis. 8 Prolonged IL-8 production by gastric epithelial cells during H. pylori infection could result in the recruitment of leukocytes to infected tissues and therefore may be important in the regulation of inflammatory and immune processes in response to H. pylori. 10 Since chronic H. pylori-associated gastritis is accompanied by monocyte and lymphocyte infiltration, in addition to neutrophil infiltration, we were interested in determining whether members of the CC subfamily of chemokines, which recruit monocytes ad lymphocytes, participated in H. pylori-associated pathogenesis.…”

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confidence: 99%

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Helicobacter pylori in a Korean isolate activates mitogen-activated protein kinases, AP-1, and NF-κB and induces chemokine expression in gastric epithelial AGS cells

et al. 2003

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Oxidant-sensitive transcription factors, nuclear factor-jB (NF-jB), and activator protein-1 (AP-1) have been considered as the regulators of inducible genes such as chemokines. Since oxygen radicals are considered as an important regulator in the pathogenesis of Helicobacter pylori (H. pylori)-induced gastric ulceration and carcinogenesis, chemokines such as interleukin-8 (IL-8) and monocyte chemoattractant protein-1 (MCP-1) may be regulated by NF-jB and/or AP-1. Ras, the upstream activator for mitogen-activated protein kinase (MAPK) and MAPK cascade regulate AP-1 activation. The present study aims to investigate whether H. pylori in a Korean isolate (HP99) induces the expression of chemokines (IL-8, MCP-1), which is regulated by Ras, MAPK, AP-1, and NF-jB in gastric epithelial AGS cells, and whether these transcriptional regulations of chemokines are inhibited by transfection with mutant genes for Ras (ras N-17), c-Jun (TAM-67), and IjBa (MAD-3) or treatment with MAPK inhibitors (U0126 for extracellular signal-regulated kinase or SB203580 for p38 kinase). In addition, virulence factors of HP99 were characterized by PCR analysis for the isolated DNA. As a result, HP99 is identified as cagA þ , vacA s1b, m2, iceA1 H. pylori strain. HP99 induced a time-dependent expression of mRNA and protein for IL-8 and MCP-1 via mediation of MAPK, AP-1, and NF-jB. Transfection with mutant genes for Ras, c-Jun, and IjBa and treatment with MAPK inhibitors suppressed H. pylori-induced activation of transcription factors (NF-jB, AP-1) and expression of chemokines (IL-8, MCP-1) in AGS cells. In conclusion, Ras and MAPK cascade may act as the upstream signaling for the activation of AP-1 and NF-jB, which induce chemokine expression in H. pylori-infected AGS cells. Specific targeting of the activation of NF-jB and AP-1 may be effective for the prevention or treatment of gastric inflammation associated with H. pylori infection.

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“…In addition, ROS activate signal transduction for the expression of inflammatory cytokines and chemokines ( 2 ). Interleukin-8 (IL-8), a member of the C-X-C chemokine family, is a potent chemoattractant and activator of neutrophils, monocytes, and T lymphocytes (3)(4)(5). ROS mediate the expression of IL-8 by activating oxidant-sensitive transcription factors in gastric epithelial cells (6)(7)(8).…”

mentioning

confidence: 99%

β-Carotene and Lutein Inhibit Hydrogen Peroxide-Induced Activation of NF-κB and IL-8 Expression in Gastric Epithelial AGS Cells

Kim

Seo

Kim

2011

J Nutr Sci Vitaminol

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Summary Reactive oxygen species (ROS) including hydrogen peroxide (H 2 O 2 ) are involved in the pathogenesis of gastric inflammation. Interleukin-8 (IL-8) is a potent mediator of the inflammatory response by activating and recruiting neutrophils to the site of infection. Oxidant-sensitive transcription factor NF-B regulates the expression of IL-8 in the immune and inflammatory events. Carotenoids (carotenes and oxygenated carotenoids) show antioxidant and anti-inflammatory activities. Low intake of ␤ -carotene leads to high risk of gastric cancer. Oxygenated carotenoid lutein inhibited NF-B activation in experimental uveitis. The present study aims to investigate whether ␤ -carotene and lutein inhibit H 2 O 2 -induced activation of NF-B and expression of IL-8 in gastric epithelial AGS cells. The cells were treated with carotenoids 2 h prior to the treatment of H 2 O 2 . mRNA expression was analyzed by reverse transcription-polymerase chain reaction (RT-PCR) and real time RT-PCR analyses. IL-8 level in the medium was determined by enzyme-linked immunosorbent assay. NF-B activation was assessed by electrophoretic mobility shift assay. ROS levels of the cells were detected by confocal microscopic analysis for fluorescent dichlorofluorescein. As a result, H 2 O 2 induced the activation of NF-B and expression of IL-8 in AGS cells time-dependently. ␤ -Carotene and lutein showed inhibitory effects on H 2 O 2 -induced increase in intracellular ROS levels, activation of NF-B, and IL-8 expression in AGS cells. In conclusion, supplementation of carotenoids such as ␤ -carotene and lutein may be beneficial for the treatment of oxidative stress-mediated gastric inflammation.

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Increased gastric production of interleukin-8 and tumour necrosis factor in patients with Helicobacter pylori infection.

Abstract: (J7 Clin Pathol 1995;48:133-136)

Cited by 139 publications

References 20 publications

Correlation of 16s rRNA with serum levels of the cytokines, TNF-α and IL-1β, in subjects with a positive Helicobacter pylori Stool Antigen test (HPSA)

Correlation of 16s rRNA with serum levels of the cytokines, TNF-α and IL-1β, in subjects with a positive Helicobacter pylori Stool Antigen test (HPSA)

Helicobacter pylori in a Korean isolate activates mitogen-activated protein kinases, AP-1, and NF-κB and induces chemokine expression in gastric epithelial AGS cells

β-Carotene and Lutein Inhibit Hydrogen Peroxide-Induced Activation of NF-κB and IL-8 Expression in Gastric Epithelial AGS Cells

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