Role of the <i>Helicobacter pylori</i>‐Induced inflammatory response in the development of gastric cancer

Lamb, Acacia; Chen, Lin Feng

doi:10.1002/jcb.24389

Cited by 163 publications

(141 citation statements)

References 64 publications

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“…Preexistent hematological conditions might be responsible for the increased risk found in these patients (34,35). The higher incidence of gastric cancer might be explained by the fact that asplenic patients are more prone to develop Helicobacter pylori infections which is a known risk factor for gastric cancer (32,36).…”

Section: Splenectomy and Cancer Riskmentioning

confidence: 99%

Patients After Splenectomy: Old Risks and New Perspectives

Dragomir¹,

Petrescu²,

Manga³

et al. 2016

chr

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Rezumat Pacienåii post-splenectomie: complicaåii cunoscute aei perspective noiComplicaåiile care survin în urma splenectomiei pot fi împãråite în infecåioase aei non-infecåioase. Legãtura dintre splenectomie aei aceste riscuri este doar paråial înåeleasã. Rãspunsul imun al gazdei împotriva infecåiei este profund modificat post-splenectomie, iar aceaeti indivizi sunt mai susceptibili sã dezvolte sepsis aei infecåia are o evoluåie fulminantã. Splenectomia este de asemenea un potenåial factor de risc pentru numeroase complicaåii vasculare care rezultã în urma obstrucåiei paråiale sau totale ale unei artere sau vene. În plus, hipertensiunea pulmonarã poate fi o complicaåie severã aei uneori fatalã a splenectomiei. Unii autori includ aei neoplaziile, diabetul zaharat aei pancreatita acutã în categoria complicaåiilor non-infecåioase post-splenectomie. Cea mai de temut complicaåie pentru pacienåii splenectomizaåi rãmâne sepsisul. Fiziopatologia sepsisului încã este controversatã. Decesul în sepsis poate surveni fie în urma hiperinflamaåiei, fie în urma imunosupresiei. Multiple dovezi experimentale au dovedit implicarea microRNA-urilor celulare aei virale în sepsis. Considerãm faptul cã microRNA-urile sunt de asemenea asociate cu imunosupresia pacientului asplenic, ceea ce determinã o creaetere a riscului de sepsis fatal. Studierea nivelului expresiei plasmatice a microRNA-urilor circulante la pacienåii asplenici, ar putea conduce la o mai bunã înåelegere a imunosupresiei post-splenectomie aei la dezvoltarea unor noi metode diagnostice aei terapeutice.Cuvinte cheie: splenectomie, microRNA, sepsis, microRNA-uri virale, OPSI AbstractThe risks that arise after splenectomy can be divided in infectious and non-infectious. The link between splenectomy and these hazards remains partially unknown. Host defense against infection is altered after splenectomy and such individuals develop sepsis more easily and the infection has a fulminant course. Splenectomy is also a potential risk factor for several vascular complications that result from partial or total obstruction of an arterial or venous blood vessel. Furthermore, pulmonary hypertensioncan be a severe and sometimes fatal complication following splenectomy. Some authors also consider that malignancies, diabetes mellitus and acute pancreatitis are non-infectious complications after splenectomy. The most feared complication for splenectomized patients remains sepsis. The pathophysiology of sepsis is still controversial. Death in sepsis can occur due to either hyper-inflammation or "immune paralysis". Multiple experimental evidences link cellular and viral microRNAs with sepsis. We presume that General ReportChirurgia (2016)

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Section: Splenectomy and Cancer Riskmentioning

confidence: 99%

Patients After Splenectomy: Old Risks and New Perspectives

Dragomir¹,

Petrescu²,

Manga³

et al. 2016

chr

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“…Helicobacter pylori (H. pylori) is a gram-negative, microaerophilic bacterium which colonizes the gastric mucosa of human (1)(2)(3) and is related with gastritis, peptic ulcer, gastric cancer, and mucosa-associated lymphoid tissue lymphoma (MALT) (4). In developing countries, H. pylori prevalence is high and approximately 70% of the people have H. pylori, while 25%-50% of the population in the developed countries is infected by H. pylori.…”

Section: Introductionmentioning

confidence: 99%

“…Chronic H. pylori infections of the stomach are a major risk factor for the development of gastroduodenal diseases. H. pylori is regarded as Class 1 carcinogen by the International Agency for Cancer Research (2,5).…”

Section: Introductionmentioning

confidence: 99%

The cytokine response in THP-1 (monocyte) and HL-60 (neutrophil-differentiated) cells infected with different genotypes of Helicobacter pylori strains

Caliskan

Sayi-Yazgan²,

Tokman³

et al. 2015

Turk J Gastroenterol

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Background/Aims: Helicobacter pylori (H. pylori) is a microaerophilic bacterium related with peptic ulcer and gastric cancer. Its virulence factors include cytotoxin-associated gene A (CagA) and vacuolating cytotoxin gene A (VacA) proteins. Cytokine release inducted by H. pylori colonization has an important role in pathogenesis of H. pylori. The severity of gastric pathologies depends on the H. pylori genotypes found in different geographical regions. We aimed to determine the relationship between different H. pylori genotypes and their effects on the cytokine release levels. Materials and Methods: ureC, cagA, vacAs1/s2, vacAm1/m2, and blood group antigen-binding adhesion protein A2 (babA2) virulence related genes were investigated in 21 H. pylori strains. Genotyping of 21 strains were made due to the presence of cagA, vacAs1/s2, vacAm1/m2, and babA2 genes. The H. pylori strains were cultured together with THP-1 and neutrophil-differentiated Human promyelocytic leukemia cells (HL-60) cells. The levels of cytokines interleukin (IL)-1β, IL-6, IL-8, IL-12, tumor necrosis factor-alpha (TNF-α), and IL-10 in these cells were measured after co-culturing with H. pylori strains. Results: The following five different genotypes were detected: Genotype1: cagA and vacAs1m2; Genotype2: cagA and vacAs1m1; Genotype3: cagA, vacAs1m2, and babA2; Genotype4: vacAs2m2; and Genotype5: cagA and vacAs2m2. All these genotypes significantly induced the levels of IL-1β, IL-6, IL-8, IL 10, and TNF-α in THP-1 cells. Genotype 5 caused higher amounts of IL-1β, IL-6, TNF-α, and IL-10, whereas genotype 1 induced the highest levels of IL-8. In neutrophil-differentiated HL-60 cells, genotype 4 increased IL-6 levels and genotype 3 and 4 elevated IL-8 levels significantly. Conclusion: These results suggested that cytokine response of the host varies depending on the specific immune response of the host against different H. pylori strains.

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“…H. pylori can either directly promote gastrointestinal carcinogenesis through the enhanced production of free radicals or indirectly through the establishment of carcinogenic environment because of longterm inflammation of the gastric mucosa, which eventually results in mucosal atrophy, intestinal metaplasia, and cancer. Accordingly, chronic inflammation caused by H. pylori is a major step in the initiation and development of gastric cancer (18). However, the exact mechanism remains unclear.…”

Section: Introductionmentioning

confidence: 99%

Uncontrolled Inflammation Induced by AEG-1 Promotes Gastric Cancer and Poor Prognosis

Zhao

et al. 2014

Cancer Research

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Gastric cancer is one of the most common causes of cancer-related death worldwide. Helicobacter pylori infection plays an important role in the development and progression of gastric cancer. The expression of astrocyte-elevated gene-1 (AEG-1) is increased in gastric cancer tissues, thereby contributing to the inflammatory response. We investigated whether and how AEG-1 regulated proinflammatory signaling in gastric cancer cells. We used human gastric cancer cell lines and athymic nude mice to investigate the role of AEG-1 in the regulation of the TLR4/nuclear factor-kB (NF-kB) signaling pathway and cancer invasion and compared the expression of AEG-1 and related proteins in 93 patients with gastric cancer by immunohistochemistry. In human gastric cancer cells, both AEG-1 and TLR4 could be induced by lipopolysaccharide (LPS) stimulation. AEG-1 was upregulated via LPS-TLR4 signaling and in turn promoted nuclear translocation of the NF-kB p65 subunit. At the same time, AEG-1 overexpression decreased the levels of suppressor of cytokine signaling (SOCS) protein SOCS-1, a negative regulator of the TLR4 pathway. Furthermore, nude mice engrafted with AEG-1/TLR4-expressing cells demonstrated larger tumor volumes than control animals. In patients with gastric cancer, the expression of AEG-1 correlated with that of TLR4, SOCS-1, and NF-kB and was higher in tumors compared with noncancerous adjacent tissues. Overall survival in patients with gastric cancer with simultaneous expression of AEG-1 and TLR4 was poor. Our results demonstrate that AEG-1 can promote gastric cancer progression by a positive feedback TLR4/NF-kB signaling-related mechanism, thus providing new mechanistic explanation for the role of inflammation in cancer progression. Cancer Res; 74(19);

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Role of the Helicobacter pylori‐Induced inflammatory response in the development of gastric cancer

Cited by 163 publications

References 64 publications

Patients After Splenectomy: Old Risks and New Perspectives

Patients After Splenectomy: Old Risks and New Perspectives

The cytokine response in THP-1 (monocyte) and HL-60 (neutrophil-differentiated) cells infected with different genotypes of Helicobacter pylori strains

Uncontrolled Inflammation Induced by AEG-1 Promotes Gastric Cancer and Poor Prognosis

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