Role of Helicobacter Pyroli Derived Factors in Cell Cycle Alteration of the Gastric Epithelial Cells

into ammonia, and thus neutralizing the surrounding acidic environment. Also, H. pylori contains "hydrogenase" enzyme, which can oxidize molecules hydrogen being produced by other gastric bacteria, in order to produce energy. Some other enzymes that can be utilized by H. pylori are "oxidase" and "catalase", which are also used to test for the presence of this organism. It can also form "biofilm" on the gastric mucosa epithelium, which results in its ability to resist against many antimicrobials. From spiral form, it is able to convert into "coccoid form" - one of its advantage which helps in its survival and epidemic potential [5].

Our world has changed dramatically since the day Antoine van Leeuwenhoek discovered microorganisms in 1676 using a simple microscope. In early days, scientists first thought life arose from inanimate materials. This theory, known as abiogenesis or spontaneous generation, was disproved later on by scientists including Lazarro Spallanzani and Louis Pasteur. The experiments conducted by these scientists showed that living things could only arise from preexisting life, or biogenesis. All life begins with a living cell, composing of five required components. These components are DNA, RNA, cell membrane, ribosome, and cytoplasm. As more investigations on bacteria were conducted, scientists were able to acquire a deeper knowledge of the microbiology and pathology of animals, plants, and humans.

H. pylori thrives in the acidic environment of the stomach and the finding that this bacteria contributed to the condition was remarkable news and led to the standard practice of treating peptic ulcers with antibiotics. As a result, the rate of H. pylori-induced ulcers has dropped by more than 50 percent. (Ackerman, 2012)

H. pylori is a narrow, curved, Gram-negative rod with polar flagella. It grows slowly in a microaerophilic atmosphere in a manner similar to Campylobacter. The bacteria have only recently be identified as the causative agent to gastric ulcers, a condition long believed to be the result of stress and lifestyle habits.

Since then, H. pylori has been almost completely eradicated in western countries, being placed onto the endangered species list. Unfortunately in developing countries, gastric and duodenal ulcers remain huge problems. The lack of access to antibiotics and the emergence of antibacterial resistant strains have greatly hindered efforts to cure the diseases. The controversy is not over, however, as 80% of people infected with H. pylori never develop any gastrointestinal diseases. We need to thoroughly research the bacterium and exactly how it works in order to fully understand the role of H. pylori in stomach diseases. With that information, we will have the means to combat the diseases caused by the bacterium and the lack of the

In the past it was believed that gastric ulcers were caused by life style modifiable risk factors. The biggest culprit now is Helicobacter pylori (H. pylori). H. Pyloris is a bacterium commonly found in the gut. The bacteria breaks down the lining of the stomach. Then the stomach acid further breaks down the lining which causes the ulcer. This is the reason, unless contraindicated, most patient receives either a Histamine-2 Receptor Antagonist or a proton pump inhibitor in the hospital. The GI symptoms that are present with gastric ulcers would decrease the appetite of the patient. Therefore the patient would encounter a digestion problem.

Helicobacter pylori is an important human pathogen that chronically infects the gastric and duodenal mucosa (1). It affects approximately 50% of the population worldwide, and is associated with multiple gastric pathologies, including gastritis, peptic ulcer disease (PUD), gastric cancer (GC) and mucosa-associated lymphoid tissue (MALT) lymphoma (2). While the majority of individuals infected with H. pylori are asymptomatic, essentially all develop chronic inflammation (3). Among infected individuals, approximately 10% develop PUD, 1-3% progresses to GC and 0.1% develop MALT lymphoma (3). Clinical outcomes of long-term infection vary, as disease severity is thought to be related to a combination of host genetics, environmental factors, and genetic heterogeneity of H. pylori (2). Helicobacter pylori exhibits a much greater genetic diversity than most bacteria, and this is often attributed to the differences in prevalence and expression of bacterial virulence factors that may impact the outcome of gastric disease (4). Several virulence genes related to the risk of gastric disease have been identified, including cagA, cagE, vacA, iceA, and babA2 (2). A large number of studies have shown that VacA producing H. pylori strains are related to more severe clinical outcomes, although the genetic mechanism(s) underlying this observed associations is not yet

Helicobacter pylori is structurally small, gram negative rods which is microaerophilic in nature and has capability of colonizing regularly in human stomach (Strausbaugh et al., 2002). Due to such colonizing capability, it is regarded as one of the most common bacterial pathogen present in almost 50% of the world’s population (Zhao et al., 2014) and the reason behind such well adaptation or enduring of H.pylori in the Human’s stomach is due to the combined effects of several factors that addresses different challenges or obstacles presented by the nasty environment inside the stomach (Montecucco and Rappuoli, 2001). Helicobacter pylori produce the urease that neutralize the gastric acid or shows the buffering effect around the surroundings within the stomach. Moreover, it has a capacity of crossing the thick mucus lining of the stomach easily and binding itself to the antigen known as Lewis antigen that are basically present in gastric cells and whose function is to secrete different factors associated with stimulating and attracting the inflammatory cells and Toxin VacA that performs the multiple functions and such activities of H.pylori is possible due to its helicoidal shape the mode of action of flagella present. Mainly, the presence of the cag pathogenicity island (Cag-PAI) which is a 40-kb DNA insertion elements containing 32 genes and encoding a type IV secretion system helps in the optimal fitness of the bacteria in the stomach and appearance of pathogenic traits.

Generally, it is through contaminated water or drinks. It is passed through fecal matter. For instance, in the event that somebody didn't wash their hands appropriately before serving you food, you could get H Pylori from it. This is a reason why you should be careful of the kind of restaurant you eat in. In addition, try to keep your home clean won’t be breeding intestinal microbes in your living room.

Explanations for the fast rise in occurrence of EAC involve the increasing prevalence of gastroesophageal reflux and obesity as well as the declining incidence of Helicobacter pylori infection. Helicobacter pylori infection is correlated with hypergastrinemia, the excess of gastrin in the blood. Gastrin is a hormone that is secreted by G cells situated in the gastric antrum and works on the parietal cells to trigger the production of hydrochloric acid. Constant hypergastrinemia due to daily PPI therapy contributes to the raised gastric acid-secretory capacity that is not obvious throughout PPI therapy, but that emerges quickly when the drug is stopped. Increased acid production due to hypergastrinemia poses a risk factor for development of

Most of the T cells in the gastric mucosa differentiate into Th1 cytokines, the others become anergic. Anergy of T cells may be brought about by the interaction of T cells with the gastric epithelial cells that express B7-H1. B7-H1 is a costimulatory molecule that increases during H. pylori infection. In gastric epithelial cells the development of Treg cells from naïve T cells is brought about by exposure to H. pylori via induction of BH-71. This suggests that H. pylori might utilise the epithelium to promote the development of Treg cells which play a vital role in suppressing effector T cells. Because of this the existence on Treg cells in H. pylori infection may diminish the adaptive immune

Identify (3) items related to the medical diagnosis that the RN can include in the teaching plan for this patient?

It is still not know exactly how H.pylori infections spread but it is know that this bacteria in particular has coexisted with humans since the very beginning of evolution. It is a common thought to most, that this bacteria is can be spread from one person’s mouth to another. Furthermore, this bacteria can be transferred from human feces to the mouth.This may occur due to the fact that many individuals fail to wash their hands thoroughly after using the bathroom. In essence, even contaminated water can cause this bacteria later resulting in a Gastric ulcer. This bacteria is capable of penetrating the stomach’s mucous lining and generating substances that can neutralize stomach acids. This resulting in a stomach cells being more vulnerable. Overall what mainly causes this bacteria to cause Gastric ulcer is how the bacteria H.pylori combined with stomach acids irritate the lining causing the sores in your stomach. The imbalance leads to inflammation which can be even worse by the use of aspirin or ibuprofen.Some risk factors also causing Gastric ulcer is Chronic gastritis, smoking, increase of age, mechanical ventilation such as a breathing machine or certain blood clotting problems. Research does not

A peptic ulcer can be defined as an “excavation that forms in the mucosal wall of the stomach, in the pylorus, in the duodenum, or in the esophagus” (Brunner, Suddarth and Smeltzer, 2008). According to Fromm, (2009) Helobactor pylori is a gram-negative bacteria that is the cause of most peptic ulcer disease and is considered a primary risk factor in the development of gastic cancer (pg. 394). Other causes include stress, and excessive secrtion of Hydrochloric acid in the stomach. Transmission of H. pylori according to Gurney, Carvalho, Gonzalez, Galaviz & Sonstein (2014) states there is strong research supporting that H. pylori can be spread person to person through direct contact with saliva, vomit, or fecal matter (pg. 393). H. Pylori is more prevalent in crowded areas without reliable access to clean water. Other risk factors include poor hygiene, smoking, and close living conditions with someone who is infected with H. pylori. Symptoms of an ulcer include a burning sensation in the stomach and esophagus, vomiting, diarrhea or constipation and bleeding. Treatment of Peptic Ulcer Disease includes antibiotics to eradicate H. pylori bacteria; proton pump inhibitors are used to treat NSAID-induced ulcers and other ulcers not associated with the bacterial infection, smoking cessation and dietary modifications. Surgical management is recommended for ulcers that fail to heal after 12-16 months of treatments and the procedures include pyloroplasy, anrectomy or vagotomy.

The bacteria causing ulcers are called Helicobacter pylori. This bacteria is infectious to the stomach because it can adapt to the stomach's acidic environment. H. pylori have flagella which help the bacteria move into the mucous lining of the stomach by burrowing. The bacteria reach the neutral environment of epithelial cells and are safe from the high acidity environment of the stomach. Once H. pylori are the lining, the epithelial cells are exposed. Normally, ammonia neutralizes the stomach acid, protecting the mucous lining from being eroded. However, ammonia is lethal to epithelial cells and causes cellular death. This cell death results in an inflammatory response (Dixon, 2001). The inflammatory response includes cellular components of the body's immune system. Once H. pylori are in the epithelial cells, infection continues to spread as H. pylori insert its DNA into the cells. Some of the DNA is replicated with the epithelial cells' DNA while other mechanisms of the cells present the inserted bacterial DNA on the cells' surface. The cells become antigen presenting cells which signal white blood cells to the site of infection (Hunt, R.H., Camilleri, M., Crowe, S. E., El-Omar, E. M., Fox, J. G., Kuipers, E. J., . Tack, J., 2015). The response also signals G cells in the stomach to secrete gastrin, and gastrin stimulates parietal cells to produce more hydrochloric acid. The excessive production of the gastric hormones further damages the site of infection, and it can also damage the duodenum of the small intestine as the acids move through the stomach (Dixon,