2005
DOI: 10.1016/j.ijmm.2005.06.003
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Adherence properties of : Impact on pathogenesis and adaptation to the host

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Cited by 83 publications
(69 citation statements)
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References 62 publications
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“…During this process, some adhesive proteins from the H. pylori membrane are affected and form a strong attachment to gastric epithelial cells (8). Outer membrane proteins, including blood group antigen-binding adhesion (BabA), adherence-associated lipoprotein A (AlpA), and adherence-associated lipoprotein B (AlpB), reportedly contribute to this process (9). Therefore, H. pylori could be eradicated by suppressing its motility or adhesion.…”
mentioning
confidence: 99%
“…During this process, some adhesive proteins from the H. pylori membrane are affected and form a strong attachment to gastric epithelial cells (8). Outer membrane proteins, including blood group antigen-binding adhesion (BabA), adherence-associated lipoprotein A (AlpA), and adherence-associated lipoprotein B (AlpB), reportedly contribute to this process (9). Therefore, H. pylori could be eradicated by suppressing its motility or adhesion.…”
mentioning
confidence: 99%
“…Attachment of Helicobacter pylori to host gastric epithelial cells is believed to play an important role in bacterial colonization and in cellular and humoral immune responses to infection (1,2). For example, direct contact between the bacteria and the epithelium is required for the release of inflammatory mediators, such as IL-8, 2 which results in the mucosal accumulation of neutrophils (3).…”
mentioning
confidence: 99%
“…For example, direct contact between the bacteria and the epithelium is required for the release of inflammatory mediators, such as IL-8, 2 which results in the mucosal accumulation of neutrophils (3).…”
mentioning
confidence: 99%
“…H. pylori that have survived the acid in the stomach are then able to negotiate the thick gastric mucous layer, courtesy of their spiral shape and multiple polar flagella (108,150). After traversing the mucous layer and reaching the gastric epithelium, H. pylori is believed to avoid being flushed away during the continual replenishment of the gastric mucosa by using a range of adhesins to tightly attach to the cells of the gastric epithelium (109). This allows H. pylori to escape the acidic conditions in the lumen of the stomach and gain access to gastric epithelial cells, which may act as a source of essential nutrients following vacuolating cytotoxin A (VacA)-dependent cell permeabilization (139).…”
Section: Colonization Of the Gastric Nichementioning
confidence: 99%