The Effects Of Helicobacter Pylori On The Human Stomach

Even though H. pylori is a "neutralophile", it can survive in the very acidic environment in the human stomach due to a variety of acidic-adaptive mechanisms, such as the ability to utilize urease to break down urea

Escherichia coli, is a gram negative, rod-shaped bacterium that can be found in the digestive tracts of humans and animals, it is an important beneficial bacteria for many organisms, it inhibits the growth of pathogenic species such as Salmonella and aids in digestion. The strains are distinguished from the presence of two surface

Gastrointestinal diseases are pervasive problem that is caused by ingestion of contaminated foods or water in which an extensive etiological agents known as enteric pathogen are present, [1]. Salmonella is one of the most opportunistic gram negative, facultative anaerobic food borne pathogens that represent a major health problem and a substantial cause of food poisoning[2]. Salmonellosis caused by Salmonella enterica serovar Typhimurium (S. Typhimurium) stance as the second most prevalent cause of acute gastroenteritis that affecting one million illnesses in the United States, with 19,000 hospitalizations and 380 deaths[3]. Infection begins with the ingestion of contaminated food or water then characterized by attachment of the bacteria by fimbriae or pili to cells lining the

Helicobacter Pylori is a disease, which if untreated can cause ulcers. My disease [Helicobacter Pylori]. This is a disease in the stomach that causes severe stomach pain. I needed tough hope to conquer my painful story of Helicobacter Pylori.

H. pylori relies heavily on the activation of the host inflammatory response in order to utilize host metabolites as well as various cytokines, and chemokines, namely IL-8. Given the knowledge on H. pylori genetic diversity, it is important to note the functionality of the cag pathogenicity island (cagPAI) encoded by H. pylori’s genome. This pathogenicity island along with the plasticity zone is a major contributor to the development of disease from pathogenic strains of the bacteria. The cag pathogenicity island also encodes for H. pylori’s Type IV secretory system used to transport virulence proteins. CagPAI activation of the inflammatory response in the stomach also results in the apoptosis of T cells. All these factors and more contribute to H. pylori’s persistence in the host and mechanisms for inducing disease. The following pages will detail how genetic diversity along with the utilization of the Type IV secretion system and vacA toxin cause such severe gastric carcinogenesis and ulcer formation, as well as the role horizontal gene transfer has on strain specific diversity and pathogenesis of

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pylori in a common infection, the host undergoes a period of rapid bacterial duplication and subsequent inflammation following colonization of the viscous mucus layer of the stomach. The penetration of the layer is assisted by the bacteria’s flagella and spiral morphology. The low oxygen level and neutral pH of the mucus act as a prime environment for the microaerophilic H. pylori. (Kusters, 2006) Preferably a lumenal pathogen, host cells are rarely invaded by the microbial. Associated with the inflammation is hypochlorhydria that can persist for months, during which the pathogen is released through fecal shedding in large amounts. After at least a few weeks, an immune response develops but it is not very effective in removing H. pylori. Eventually the inflammation subsides to a stable state and the infection becomes asymptomatic but may persist for decades. (Blaser,

The infection process is very complex due to numerous virulent factors of the pathogen. In order to enter the small intestine a bacterium must first overcome the antimicrobial activity of saliva enzyme, lactoperoxidase and the low pH of digestive fluid in the (D 'Aoust, 1991). Cytotoxin present on the bacterial cell wall disturb membrane integrity of the host cells which contribute to bacterium attachment and to cell invasion (D 'Aoust, 1991). Salmonella attaches itself to the intestinal epithelial cells by fimbriae. Pathogens enter epithelial cells by membrane-bound vesicle, this process is known as bacteria-mediated endocytosis (D 'Aoust, 1991). Bacterium then divide and invade mucosa layer. Diarrheagenic enterotoxin is released in the intestinal lumen and into the lumen of epithelial cells. Effect of enterotoxin and local inflammation cause water and

The simulated gastric solution consisted of distilled water containing 0.2% NaCl with its pH adjusted to 1.5 by 5 M HCl; the solution was filter-sterilized using a 0.2 mm filter (Cook et al. 2011; Mokarram et al. 2009; Rao et al. 1989). The assay was initiated by transferring the produced beads (uncoated, coated) to 9 mL of simulated gastric solution; the initial cell concentration was approximately 8.8× 1013 CFU/mL and 2 -6 × 1012 (uncoated, coated beads). The suspension was incubated at 37° C; samples were collected at 0, 60, and 120 min and following the incubation, the beads were removed. Viable cells of each bacterium were then enumerated in triplicates using method described in Section 2.5 and the counts were expressed as mean log CFU/mL.

However, pregnancy might make connected with an expanded likelihood to H. Pylori spoiling and it need been hypothetically recommended that a progress clinched alongside gastrointestinal tract ph Throughout right on time pregnancy Similarly as an aftereffect from claiming expanded amassing from claiming woman’s constitution fluid, steroid hormone changes, Furthermore immunologic tolerance, Might lead the actuation for idle H. Pylori infection, which could overstate those indications of queasiness What's more spewing (Guven et al. ,

coli is a gram negative bacterium that is a normal inhabitant of the digestive tracts of humans and animals. It is a beneficial bacteria that inhibit the growth of pathogenic species such as Salmonella. The strains are distinguished by the presence of two surface antigens: O, and outer-membrane antigen and H, an antigen on the flagellum (Meyer, R. R., 2015). It is a model organism, therefore it is a fast and efficient organism for biological research. It gains this from its simplicity as a single celled organism, its quick reproduction rate, adaptivity, and is harmless in most naturally occurring strains (study.com).

As there are many causes of peptic ulcer disease, the number one causative agent is a Helicobacter pylori infection. This spiral shaped bacterium was known as far back as 1875. It was discovered that this bacteria inhabited the lining of the human stomach by German scientists. Unfortunately it was impossible to culture at the time so it fell by the wayside and was forgotten ( Hardy, J ). It wasn’t until 1979 that an Australian pathologist Robin Warren noticed that many of his patients who were suffering from gastric ulcers had mysterious bacteria clinging to the tissues of his biopsy specimens. He alongside with his associate physician Barry Marshall, worked endlessly to culture what they saw under the microscope. It was by accident in 1982 that they left their cultures incubating over a five day span and what they discovered upon returning

Prevalence of duodenal and gastric ulcers in patients with liver cirrhosis increases as the disease progress[11] and this prevalence becomes higher in decompensated cirrhosis than in compensated cirrhosis [12]. Currently, PPIs are the mainstay treatment option of peptic ulcers in the general population [13]. Helicobacter pylori infection contributes to the development of hyperammonemia [14] and subsequent episodes of

The organism responsible for this disease is a strain of E.coli called E.coli 0157:H7. E.coli is a gram-negative rod that inhabit the human gastrointestinal track and mostly harmless. However, the strain 0157 can produce powerful toxins that can lead to severe cases of food poisoning (Gould, 2010). The bacteria were first identified as a cause of foodborne illness in 1982 when an outbreak of

Antibiotic therapy, although effective, is associated with several disadvantages including the low patient compliance due to the drugs’ side effects, treatment failure as a result of the emergence of drug-resistant strains, high costs, and the failure to prevent reinfection [4-7]. Therefore, alternative approaches to combat H. pylori infection are currently pursued, including vaccination. Several H. pylori proteins have been identified as immunogenic in preclinical models, including Urease B (UreB) [8], Vacuolating toxin A (VacA) [9], H. pylori adhesion A (HpaA) [10], neutrophil-activating protein A (NapA) [11], outer membrane protein (Omp) [12], cytotoxin-associated antigen (CagA) [9], heat-shock proteins (Hsp) [13, 14], OipA [15] catalase [16] and chimeric genes [17-19]. Each of these antigens has the ability to reduce the bacterial load in animal models, but none affords protection against infection. Current strategies to enhance vaccine efficacy include the identification of most suitable immune targets and the combination of immunodominant antigens into multivalent formulations. Gholi et al. [20] demonstrated that FliD,, the flagellar hook-associated protein 2, reacts with approximately 97 percent of sera obtained from patients infected with H. pylori, suggesting that this is a common immune target in the infected human host [20]. FliD plays a crucial role in flagella assembly. Flagellin is important for bacterial motility and is essential for