&lt;i&gt;Helicobacter pylori&lt;/i&gt; Eradication Induced Constant Decrease in Interleukin- 1B Expression over More Than 5 Years in Patients with Gastric Cancer and Dysplasia

Kim, Hee Jin; Kim, Nayoung; Park, Ji Hyun; Choi, Sunkyu; Shin, Cheol Min; Lee, Ok Jae

doi:10.5009/gnl19312

Cited by 10 publications

(5 citation statements)

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“…Interleukin‐1β (IL‐1β) is a quintessential pro‐inflammatory cytokine expressed primarily by monocytes and macrophages. The biological functions of IL‐1β mainly include mediating inflammatory responses and innate immunity, 1 and IL‐1β's ability to induce DNA methylation is closely related to the occurrence and development of tumors 2,3 . In addition, with the discovery of the relationship between osteoarthritis and IL‐1β‐induced chondrocyte apoptosis, 4 there is increasing evidence that IL‐1β can induce apoptosis, such as cardiomyocyte, 5 nucleus pulposus cells, 6 human umbilical vein endothelial cells, 7 β‐cells, 8 and fibrosus cells 9 …”

Section: Introductionmentioning

confidence: 99%

“…The biological functions of IL-1β mainly include mediating inflammatory responses and innate immunity, 1 and IL-1β's ability to induce DNA methylation is closely related to the occurrence and development of tumors. 2,3 In addition, with the discovery of the relationship between osteoarthritis and IL-1βinduced chondrocyte apoptosis, 4 there is increasing evidence that IL-1β can induce apoptosis, such as cardiomyocyte, 5 nucleus pulposus cells, 6 human umbilical vein endothelial cells, 7 β-cells, 8 and fibrosus cells. 9 Apoptosis is the autonomous and orderly death of cells under certain physiological or pathological conditions, which is controlled by a series of activation, expression, and regulation of genes.…”

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confidence: 99%

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Role of signal transduction pathways in IL‐1β‐induced apoptosis: Pathological and therapeutic aspects

Wang

Qian

Xiao

et al. 2023

Immunity Inflam & Disease

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Background: Interleukin-1β (IL-1β) is a pro-inflammatory cytokine mainly produced by monocytes and macrophages with a wide range of biological effects. Evidence has shown that IL-1β plays a vital role in the process of apoptosis; however, the specific mechanisms, by which IL-1β induces apoptosis, vary due to different cellular and experimental conditions. Therefore, this present reviewstudy aimed to systematically review the association between the molecular mechanisms of IL-1β-induced apoptosis in pathological processes and the role of signaling pathways. This article also sought to briefly investigate the potential of signaling pathway-targeted therapy in the prevention and treatment of disease. Methods: This is a literature review article. The present discourse aim is first to scrutinize and assess the available literature on IL-1β and apoptosis. The relevant studies using the keywords of "IL-1β-induced apoptosis" and "signaling pathways" were searched in the databases of PubMed, Scopus, Google Scholar, and Web of Science. Gathered relevant material, and extracted information was then assessed. Results: IL-1β can induce apoptosis in various types of cells under different external stimuli via the mitochondrial pathway, death receptor pathway and endoplasmic reticulum pathway, and that the different pathways are often interconnected. The NF-KB signaling pathway, p38MAPK, and JNK signaling pathways mainly play a proapoptotic part, and the ERK1/2 pathway has a bidirectional role in regulating apoptosis, while activation of the PI3K-Akt signaling pathway can inhibit apoptosis. Conclusion: This review indicates that IL-1β-induced apoptosis plays an important role in pathogenesis and development of pathology of many inflammatory diseases. Elucidating the role of the signaling pathways will aid the development of targeted therapeutic treatments.

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Section: Introductionmentioning

confidence: 99%

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confidence: 99%

Role of signal transduction pathways in IL‐1β‐induced apoptosis: Pathological and therapeutic aspects

Wang

Qian

Xiao

et al. 2023

Immunity Inflam & Disease

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“…Second, we did not measure cytokine levels from gastric juice or plasma. However, the measurement of mRNA expression levels of cytokine genes from gastric mucosal samples may also provide meaningful results [ 39 , 40 ]. Third, our findings were not validated in different ethnic populations.…”

Section: Discussionmentioning

confidence: 99%

Altered Gastric Microbiota and Inflammatory Cytokine Responses in Patients with Helicobacter pylori-Negative Gastric Cancer

Kim

Jacobs

et al. 2022

Nutrients

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The role of the gastric mucosal microbiome in Helicobacter pylori-negative gastric cancer (GC) remains unclear. Therefore, we aimed to characterize the microbial alterations and host inflammatory cytokine responses in H. pylori-negative GC. Gastric mucosal samples were obtained from 137 H. pylori-negative patients with GC (n = 45) and controls (chronic gastritis or intestinal metaplasia, n = 92). We performed 16S rRNA gene sequencing (n = 67), a quantitative reverse transcription-polymerase chain reaction to determine the relative mRNA expression levels of TNF (tumor necrosis factor), IL1B (interleukin 1 beta), IL6 (interleukin 6), CXCL8 (C-X-C motif chemokine ligand 8), IL10 (interleukin 10), IL17A (interleukin 17A), TGFB1 (transforming growth factor beta 1) (n = 113), and the correlation analysis between sequencing and expression data (n = 47). Gastric mucosal microbiota in patients with GC showed reduced diversity and a significantly different composition compared to that of the controls. Lacticaseibacillus was significantly enriched, while Haemophilus and Campylobacter were depleted in the cancer group compared to the control group. These taxa could distinguish the two groups in a random forest algorithm. Moreover, the combined relative abundance of these taxa, a GC microbiome index, significantly correlated with gastric mucosal IL1B expression, which was elevated in the cancer group. Overall, altered gastric mucosal microbiota was found to be associated with increased mucosal IL1B expression in H. pylori-negative GC.

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“…Colonization of the gastric mucosa by Hp causes acute diffuse inflammation followed by chronic inflammation. Bacterial virulence and host genetic factors determine the severity and pathological sequelae of inflammation 4 . Once Hp successfully colonizes the gastric epithelium, the bacterial toxin CagA is injected into the host epithelial cells through the type IV secretion apparatus causing the ‘hummingbird phenotype’ 5,6 .…”

Section: Introductionmentioning

confidence: 99%

“…Bacterial virulence and host genetic factors determine the severity and pathological sequelae of inflammation. 4 Once Hp successfully colonizes the gastric epithelium, the bacterial toxin CagA is injected into the host epithelial cells through the type IV secretion apparatus causing the 'hummingbird phenotype'. 5,6 The morphological changes characteristic of this phenotype are associated with…”

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confidence: 99%

Effect of Helicobacter pylori infection and its eradication on the expression of tight junction proteins in the gastric epithelium in relation to gastric carcinogenesis

et al. 2022

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Background Tight junction proteins (TJPs) play a role in epithelial defense mechanisms. However, the effect of Helicobacter pylori (Hp) on TJPs remains unclear. This study aimed to evaluate the expression of TJPs in relation to Hp infection and eradication in gastric carcinogenesis. Methods In total, 510 subjects (284 controls and 226 gastric cancer [GC] patients) were prospectively enrolled in the study. The expression of claudin‐1 and ‐2 (CLDN‐1, ‐2), occludin (OCLN), and tight junction protein 1 (TJP1) was measured based on their Hp infection status in normal corpus mucosa and evaluated following Hp eradication using quantitative real‐time polymerase chain reaction (qPCR) and immunohistochemistry (IHC). Results The expression of TJP1 in Hp+ controls was significantly lower than that in Hp− controls (p = 0.006), whereas it was higher in Hp+ than in Hp− GC patients (p = 0.001). Moreover, the increased expression of TJP1 in Hp+ GC patients was reduced to levels in Hp−within a year after Hp eradication and was maintained for more than 5 years. Furthermore, IHC results for TJP1 were similar to qPCR results. In particular, the higher IHC staining intensity of TJP1 in the cytosol of GC patients (p = 0.019) decreased after Hp eradication (p = 0.040). Conclusion Hp infection affects TJP expression. The high expression of TJP1 in Hp+ GC patients was restored to control levels after Hp eradication, suggesting that TJP1 plays a role in gastric carcinogenesis.

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<i>Helicobacter pylori</i> Eradication Induced Constant Decrease in Interleukin- 1B Expression over More Than 5 Years in Patients with Gastric Cancer and Dysplasia

Abstract: IM-negative subjects. The continuous reduction in the IL-1B mRNA level in patients with GC/dysplasia after Hp eradication contributes to the prevention of metachronous GC after Hp eradication.

Cited by 10 publications

References 34 publications

Role of signal transduction pathways in IL‐1β‐induced apoptosis: Pathological and therapeutic aspects

Role of signal transduction pathways in IL‐1β‐induced apoptosis: Pathological and therapeutic aspects

Altered Gastric Microbiota and Inflammatory Cytokine Responses in Patients with Helicobacter pylori-Negative Gastric Cancer

Effect of Helicobacter pylori infection and its eradication on the expression of tight junction proteins in the gastric epithelium in relation to gastric carcinogenesis

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