A role for altered phagosome maturation in the long-term persistence ofHelicobacter pyloriinfection

Abstract

<jats:p>The vigorous host immune response that is mounted against Helicobacter pylori is unable to eliminate this pathogenic bacterium from its niche in the human gastric mucosa. This results in chronic inflammation, which can develop into gastric or duodenal ulcers in 10% of infected individuals and gastric cancer in 1% of infections. The determinants for these more severe pathologies include host (e.g., high IL-1β expression polymorphisms), bacterial [e.g., cytotoxicity-associated gene ( cag) pathogenicity island], and environmental (e.g., dietary nitrites) factors. However, it is the failure of host immune effector cells to eliminate H. pylori that underlies its persistence and the subsequent H. pylori-associated disease. Here we discuss the mechanisms used by H. pylori to survive the host immune response and, in particular, the role played by altered phagosome maturation.</jats:p>

Helicobacter pylori Infection in a Pig Model Is Dominated by Th1 and Cytotoxic CD8+T Cell Responses

“…More specifically, H. pylori not only was localized to murine gastric epithelial progenitor cells (48) but also was identified in human tissue specifically residing within gastric epithelial cells, parietal cells, and lamina propria macrophages (49,50). In macrophages, some H. pylori strains have the ability to prevent phagosome maturation, allowing the bacterium to survive and replicate by escaping phagocytic killing (51,52). Furthermore, H. pylori has been found in gastric lymph nodes, suggesting lymphatic dissemination (49).…”

Low-dose Aspirin and Comorbidities are Significantly Related to Bleeding Peptic Ulcers in Elderly Patients Compared with Nonelderly Patients in Japan

“…It is well documented that Helicobacter pylori infection is one of the most important causes of peptic ulcers (1)(2)(3). Nonsteroidal anti-inflammatory drugs (NSAIDs), aspirin and corticosteroids are important and exacerbating factors of bleeding peptic ulcers (4)(5)(6).…”

Investigating the Role of Helicobacter pylori PriA Protein

“…H. pylori has developed a battery of antioxidant proteins such as superoxide dismutase, catalase, and peroxiredoxins that enable it to avoid oxidative destruction [56]. In addition to diverse oxidant detoxification enzymes and potent acid-avoidance mechanisms, efficient DNA repair systems are required for H. pylori to survive in the host [56,57]. In addition to diverse oxidant detoxification enzymes and potent acid-avoidance mechanisms, efficient DNA repair systems are required for H. pylori to survive in the host [56,57].…”

“…Urease hydrolyzes urea to yield ammonium ions and thereby contributes to the acid resistance of H. pylori [4]. In addition to diverse oxidant detoxification enzymes and potent acid-avoidance mechanisms, efficient DNA repair systems are required for H. pylori to survive in the host [56,57]. To repair DNA double-strand breaks and blocked replication forks, H. pylori is equipped with an efficient system of DNA recombinational repair.…”