Helicobacter pylori-induced gastric inflammation and gastric cancer (original) (raw)
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Helicobacter pylori induced gastric cancer
Gastric cancer is one of the most common cancer-related deaths worldwide. Helicobacter pylori has been recognized as one the most important etiologic agents in the development of gastric cancer. A number of virulence factors, that are utilized by this pathogen to establish and to maintain colonization of the stomach, have been investigated to date: adhesion proteins, urease, CagA, VacA, and outer membrane vesicleswhich all not only help the bacterium to maintain its gastric niche, but also to escape the damaging response from the immune system. Standard treatment protocols have been developed for eradication of this infection; however, the treatment failure and reinfection rates are still quite high, particularly, due to the formation of biofilms by this pathogen. Therefore, it might be reasonable to explore the strategies to combat biofilm formation in the stomach in order to improve the success rates of the conventional therapies and to possibly prevent the development of gastric cancer. This review will focus on the virulence factors that are employed by the pathogen, on its interaction with the host immune system, and on conventional treatment protocols, as well as on biosurfactant agents and natural supplements that can be possibly used for biofilm destruction in stomach.
Helicobacter pylori: pathological mechanism involved in gastric colonization
Romanian journal of internal medicine = Revue roumaine de médecine interne, 2009
Since 1982, when Marshall and Warren highlighted the presence of H. pylori at the apical pole of the epithelial gastric cells, the medical literature has registered a cascade of subsequent researches concerning this amazing bacterium, its action on the human body and the body response. The apogee of these studies and conclusions about the pathogenic role of HP was touched with its certain recognition as class one carcinogenic agent (Peura 1997, WHO), becoming the first bacteria with such an action. The data gathered in the last period identify different virulence factors of HP, but fail to fully explain the relatively low incidence of gastric cancer in HP carriers; therefore, it is now considered that the carcinogenic potential related to HP infection in humans is due to the synergic and complementary association of the bacterial genetic equipment with diet and host response.
Helicobacter pylori Infection - An Up to Date on the Pathogenic Mechanisms, Diagnosis and Clinical Management [Working Title]
The discovery that Helicobacter pylori was the dominating cause of gastritis is among the most important findings in the last century. It gave rise to the understanding and treatment of serious and common diseases, such as peptic ulcer disease and gastric cancer. The gastric hormone gastrin is involved in the pathogenesis of both duodenal ulcer and gastric cancer, whereas reduction in the defense mechanism (mucus and bicarbonate) by the inflammation itself predisposes to gastric ulcer. The search for carcinogenic H. pylori factors has been unsuccessful and based upon the fact that H. pylori predispose to gastric cancer only after having induced oxyntic atrophy is an important argument in favor of a central role of gastrin increase secondary to reduced acidity. The only cell with an undisputed gastrin receptor is the enterochromaffin-like cell where gastrin has a trophic effect leading to hyperplasia, neuroendocrine tumor (NET), and long-term carcinoma of diffuse type. H. pylori may ...
Helicobacter pylori and gastric cancer
The American Journal of Medicine, 1999
Helicobacter pylori (H. pylori) is one of the most common infectious diseases worldwide. There are data on the epidemiology, pathophysiology, and histology of this disease that show that H. pylori gastritis has an important role in gastric carcinogenesis. However, it has to be considered that only very few of those infected with H. pylori will develop gastric cancer. Hence, it will be a main target of future research to identify individuals who carry a greater risk for developing gastric cancer, and therefore may benefit from eradication of H. pylori in terms of gastric cancer prevention.
Host pathogen interactions in Helicobacter pylori related gastric cancer
World Journal of Gastroenterology, 2017
Helicobacter pylori (H. pylori), discovered in 1982, is a microaerophilic, spiral-shaped gram-negative bacterium that is able to colonize the human stomach. Nearly half of the world's population is infected by this pathogen. Its ability to induce gastritis, peptic ulcers, gastric cancer and mucosa-associated lymphoid tissue lymphoma has been confirmed. The susceptibility of an individual to these clinical outcomes is multifactorial and depends on H. pylori virulence, environmental factors, the genetic susceptibility of the host and the reactivity of the host immune system. Despite the host immune response, H. pylori infection can be difficult to eradicate. H. pylori is categorized as a group Ⅰ carcinogen since this bacterium is responsible for the highest rate of cancerrelated deaths worldwide. Early detection of cancer can be lifesaving. The 5-year survival rate for gastric cancer patients diagnosed in the early stages is nearly 90%. Gastric cancer is asymptomatic in the early stages but always progresses over time and begins to cause symptoms when untreated. In 97% of stomach cancer cases, cancer cells metastasize to other organs. H. pylori infection is responsible for nearly 60% of the intestinaltype gastric cancer cases but also influences the development of diffuse gastric cancer. The host genetic susceptibility depends on polymorphisms of genes involved in H. pylori-related inflammation and the cytokine response of gastric epithelial and immune cells. H. pylori strains differ in their ability to induce a deleterious inflammatory response. H. pylori-driven cytokines accelerate the inflammatory response and promote malignancy. Chronic H. pylori infection induces genetic instability in gastric epithelial cells and affects the DNA damage repair systems. Therefore, H. pylori infection should always be considered a pro-cancerous factor.
Helicobacter pylori infection and gastric carcinoma
Clinical Microbiology and Infection, 2015
Helicobacter pylori infection is considered to be the main cause of gastric cancer and the most frequent infection-induced cancer. H. pylori is a heterogeneous species which can harbour pathogenic factors such as a cytotoxin, a pathogenicity island (cag) encoding a type 4 secretion system, and the first bacterial oncoprotein, CagA. This oncoprotein appears to be involved in the carcinogenic process in addition to the inflammation generated. This process may concern either local progenitors via an epithelial-mesenchymal transition, or recruited bone marrow-derived mesenchymal cells. There are also environmental factors such as iron deficiency or high-salt diets which interact with the bacterial factors to increase the risk of gastric cancer as well as genetic polymorphism of certain cytokines, e.g. IL-Iβ. Recent data suggest that a break in coevolution of a particular phylogeographic lineage of H. pylori and its usual host may also be a risk factor. Studies are currently being performed to assess the feasibility of organized H. pylori eradication programmes to prevent gastric cancer.
The Role of Helicobacter Pylori Virulence Factors in Gastric Cancer
Multidisciplinary Cancer Investigation
Introduction: Gastrointestinal (GI) cancers are considered among the most important causes of mortality and morbidity. Helicobacter pylori infection has been proven to be highly associated with the development of a variety of gastric diseases such as chronic gastritis, peptic ulcer disease (PUD), mucosa-associated lymphoid tissue (MALT), and gastric cancer (GC). To date, the exact role of the virulence factors in gastric diseases and other diseases remains elusive and controversial. Methods: The present study is a classic systematic review (expert opinion), in which articles published in English and Persian languages derived from Web of Science, Scopus, PubMed, and Iranian databases, including Magiran, IranMede, and scientific information database (SID) without any time limitation were explored using standardized keywords of H. pylori, virulence factors, gastric cancer, a combination of the above words, and other synonymous keywords. Finally, the information and obtained results were collected and interpreted. Results: In total, 14 of the 172 articles reviewed had inclusion criteria with the approval of the responsible author. According to the results, the development of chronic bacterial inflammation due to pathogenic mechanisms and factors, especially the role of cagA and vacA genes in gastric cancer, remains an important medical problem. Conclusions: Each of the H. pylori virulence factors can have a role in cancer development, and it appears that on-time H. pylori treatment is one of the best methods to prevent gastric cancer. Therefore, targeting Pathogenic factors of H. pylori to induce apoptosis and stimulate the immune system will be a promising, attractive, and helpful method for cancer prevention.
Helicobacter pylori and gastric malignancies
Helicobacter, 2002
Clinical outcomes of Helicobacter pylori infection are diverse and caused by the variability of H. pylori virulence factors, host susceptibility, environmental factors and their interactions. Prospective epidemiological studies have clearly shown the relationship between H. pylori infection and gastric cancer. In addition, studies in animal models such as Mongolian gerbils with or without the addition of low-dose chemical carcinogens demonstrated that H. pylori infection can develop gastric carcinoma. Experimental studies have shown that virulence factors of H. pylori interact with gastric epithelial cell signaling related to carcinogenesis.
Helicobacter pylori and Its Role in Gastric Cancer
Microorganisms
Gastric cancer is a challenging public health concern worldwide and remains a leading cause of cancer-related mortality. The primary risk factor implicated in gastric cancer development is infection with Helicobacter pylori. H. pylori induces chronic inflammation affecting the gastric epithelium, which can lead to DNA damage and the promotion of precancerous lesions. Disease manifestations associated with H. pylori are attributed to virulence factors with multiple activities, and its capacity to subvert host immunity. One of the most significant H. pylori virulence determinants is the cagPAI gene cluster, which encodes a type IV secretion system and the CagA toxin. This secretion system allows H. pylori to inject the CagA oncoprotein into host cells, causing multiple cellular perturbations. Despite the high prevalence of H. pylori infection, only a small percentage of affected individuals develop significant clinical outcomes, while most remain asymptomatic. Therefore, understanding...