H.Pyloric is Carcinogenic due to all Except
Gastric infection with the bacterium H. pylori accounts for the majority of Peptic Ulcer Diseases. This organism also plays a role in the development of gastric mucosa-associated lymphoid tissue (MALT) lymphoma and gastric adenocarcinoma. It is a gram-negative microaerophilic rod found most commonly in the deeper poions of the mucous gel coating the gastric mucosa or between the mucous layer and the gastric epithelium. The paicular end result of H. pylori infection (gastritis, PUD, gastric MALT lymphoma, gastric cancer) is determined by a complex interplay between bacterial and host factors. Bacterial factors: H. pylori is able to facilitate gastric residence, induce mucosal injury, and avoid host defense. Different strains of H. pylori produce different virulence factors. A specific region of the bacterial genome, the pathogenicity island (cag-PAI), encodes the virulence factors Cag A and pic B. Vac A also contributes to pathogenicity, although it is not encoded within the pathogenicity island. These virulence factors, in conjunction with additionalbacterial constituents, can cause mucosal damage, in pa through their ability to target the host immune cells. Host factors: Elevated concentrations of multiple cytokines are found in the gastric epithelium of H. pylori-infected individuals, including interleukin (IL) 1a/b, IL-2, IL-6, IL-8, tumor necrosis factor (TNF) a, and interferon (IFN) g. H. pylori infection also leads to both a mucosal and a systemic humoral response, which does not lead to the eradication of the bacteria but fuher compounds epithelial cell injury. Ref: Harrison&;s Principles of Internal Medicine; 19th edition; Chapter 348 Peptic Ulcer Disease and Related Disorders; Page no: 1917
Cag A gene
Vac A gene
Elaboration of interleukin 8
Causes RNA splicing
Bacteriology