The GI tract functions as an essential boundary
The GI tract functions as an essential boundary between microbial populations and human hosts. The tract keeps the two from getting in touch, which could cause health problems. According to Kusters, van Vliet, and Kuipers (2006), one of the possible outcomes of the two interacting is the development of mucosal inflammation. Helicobacter pylori infection is an example of a microbial-host interaction infection (H. pylori). H. pylori is a gram-negative bacterium that attacks both humans' and primates' stomachs, according to Kusters, van Vliet, and Kuipers (2006). The infection mechanism entails the induction of chronic gastritis in all hosts. Kusters, van Vliet, and Kuipers (2006) affirmed that the process increases the risks of developing ulcers. This paper discusses the pathogenesis of helicobacter pylori and how it causes ulcers.
Pathogenesis of Helicobacter Pylori
Helicobacter pylori (H. pylori) have various virulence molecules. These include cytotoxin, neutrophil activating protein (NAP), and lipopolysaccharide (LPS). However, Cag Pathogenicity Island (CagPAl), a combination of Cag genes (CagL, CagE, and CagH) is the primary virulence element of helicobacter pylori (Kusters, van Vliet, & Kuipers, 2006). The bacteria enter the gastric lumen at the point where the urease facilitates continued existence in the acidic context by releasing molecules of ammonia during infection. The molecules buffer periplasmic and cytosolic pH around the bacterium.
Epithelial cells and bacterial interaction
Epithelial cells which coat the gastric mucosal act as the first point of contact between helicobacter pylori and the host. According to Kusters, van Vliet, and Kuipers (2006), flagella drive the helicoidal bacterium through the mucous layer to the gastric epithelial cells. The bacteria stick to the cells using unique adhesions and then induce the CagA protein into the cells around through Type IV secretion system. The system also releases other toxic elements such as Helicobacter pylori NAP and VacA. Price and Frey's (2003) research shows that VacA initiates development of vacuoles.
Inflammatory response and ulcers
H. pylori-NAP penetrates the epithelial membrane and also introduces monocytes and neutrophils that damage tissue through reactive oxygen intermediates (ROIs). Kusters, van Vliet, and Kuipers (2006) add that injected Cag proteins lead to changes in the formation of cytoskeleton and then signals the nucleus to produce inflammatory lymphokines that accelerate inflammation through addition of lymphocytes. The proteins also induce release of ROIs. According to Kusters, van Vliet, and Kuipers (2006), combination of VacA and ROIs toxic activities results in damage of tissue which accelerated by weakening of the protective layer of mucus and permeation of acid.
Other mechanisms and effects
VacA further penetrates the mitochondrial membranes and initiates the release of cytochrome-C (Cytoc) (Kusters, van Vliet, & Kuipers, 2006; Sutton & Mitchell, 2010). Another mechanism through which helicobacter can lead to apoptosis is through inducing cell-surface receptor called Fas Ligand. The pathogen might also lead to major histocompatibility complex II (MHC-II) molecules found on the surface of the gastric epithelial cells. As a result, they induce the apoptosis (Stoker, 2013). Helicobacter porins and urease might also contribute to neutrophils chemotaxis.
Gastric epithelium and immune response
Gastric epithelium of people infected with helicobacter pylori has tumor necrosis factor alpha (TNF-Alpha) among other elements. However, IL-8, a strong neutrophil activating chemokine demonstrated by the cells of gastric epithelial, play the leading role (Kusters, van Vliet, & Kuipers, 2006). Nonetheless, helicobacter pylori strain accompanied by Cag-PAN introduce a stronger IL-8 response compared to Cag-negative strains (Kusters, van Vliet, & Kuipers, 2006). However, the response depends on the early-response transcription aspect called Activating Protein and activation of nuclear factor-kappaB (NF-KappaB). Macrophage, which is also involved in the production of IL-8 induces inflammatory cytokines responsible for the activation of the induced cells particularly T Helper cells (Whitney & Rolfes, 2008). In turn, the TH1 cytokines and Interferon-Gamma lead to the development of MHC-II, B7-1, and B7-2 accessory molecules through epithelial cells which prepare them for presentation of antigen.
Disruption of the epithelial barrier and gastric ulcers
The cytokine Fas together with VacA-mediated apoptosis stimulated by TNF-Alpha disrupt the epithelial barrier. TNF-Alpha then assists in movement of bacterial antigens and the development of macrophages (Sutton & Mitchell, 2010). According to Kusters, van Vliet, and Kuipers (2006), cytokines induced by macrophages might also alter mucus secretion hence contributing disruption of the mucus layer mediated by helicobacter pylori. Most importantly, Ifn-Gamma, IL-1 Beta, and TNF-Alpha accelerate release of gastrin, cause changes in the mucus glycoprotein, and induces secretion of enterochromaffin and parietal cells. In addition, TNF-Alpha induces a decline in the quantity of antral D cells thus causing decreased production of somatostatin and indirectly increasing production of gastric acid (Sutton & Mitchell, 2010). These and other conditions the bacteria create in the body make it vulnerable to duodenal and gastric ulcers.
Ulcers
Ulcers are a lesion or sores which mainly occur in a digestive system. According to Kusters, van Vliet, and Kuipers (2006), gastric ulcers which affect the stomach lining and duodenum ulcers that occur in small intestine are the two common types of ulcers. The problem results from compromised lining of the stomach or small intestine which leaves them unprotected and exposed to gastric juices.
How Helicobacter Pylori Causes Ulcers
Helicobacter resides in the space between epithelial cells and mucus which protects the cells. The mechanism through which helicobacter pylori causes ulcers has not been precisely established. However, the most likely mechanisms include enzymatic degradation of the mucus layer that protects stomach or small intestine, increase in cytotoxin which damages mucosal cells and other inflammatory cells in its response to the presence of the bacterium (Lehne, 2013; Sutton & Mitchell, 2010). In addition, helicobacter produces urease, an enzyme which produces carbon IV oxide and ammonia from urea in gastric juice. The two compounds are harmful to gastric mucosa.
The bacterium escapes destruction by pepsin and acid and colonizes stomach and duodenum thus compromising their lining and exposes them to acid. According to Lehne (2013), acid causes ulcers by directly injuring the gastrointestinal mucosa cells and then indirectly activating pepsin. Pepsin is a proteolytic enzyme found in gastric juice. Lehne (2013) warns that just like gastric acid, pepsin can damage unprotected duodenum mucosa and gastric cells. The presence of helicobacter pylori also causes ulcers by exposing an individual to zollinger-ellison syndrome. This is the main disorder in which excessive secretion of acid alone causes ulcers. According to Lehne (2013), zollinger-ellison syndrome results from tumor which secretes gastrin, a hormone that stimulates production of gastric acid. The acid is produced in large quantity thus making it overwhelm mucosal defense. Nonetheless, Zollinger-Ellison causes less than 0.1 percent of duodenal ulcers. Essentially, damage of stomach and duodenum lining exposes these body parts to a number of conditions.
Conclusion
Helicobacter pylori reside in the body for a long time because it can survive in acidic conditions. The bacterium causes ulcers by weakening duodenum and stomach lining thus exposing them to gastric juices.
References
Kusters, J. G., van Vliet, A. H., & Kuipers, E. J. (2006). Pathogenesis of Helicobacter pylori infection. Clinical Microbiology Reviews, 19(3), 449-490.
Lehne, R. A. (2013). Pharmacology for nursing care. St. Louis, Mo: Elsevier/Saunders.
Price, P., & Frey, K. B. (2003). Microbiology for surgical technologists. Australia: Thomson/Delmar Learning.
Stoker, H. S. (2013). General, organic, and biological chemistry. Australia: Brooks/Cole Cengage Learning.
Sutton, P., & Mitchell, H. M. (2010). Helicobacter pylori in the 21st Century. Wallingford, Oxfordshire, U.K: CAB International.
Whitney, E. N., & Rolfes, S. R. (2008). Understanding nutrition. Belmont, CA: Thomson/Wadsworth.
