Helicobacter pylori intragastric colonization and migration: Endoscopic manifestations and potential mechanisms

Table 1 The mechanisms of common endoscopic features

Endoscopic features	Mechanisms
Nodularity	Follicular lymphoid hyperplasia with intraepithelial lymphocytosis[47]; Superficially located, enlarged hyperplastic lymphoid follicles[48]; Increased numbers of MECA-79 HEV-like vessels[48]; Th2 immune response[49]
Diffuse redness	Infiltration of neutrophils and monocytes[44,58]
Spotty redness	Unclear
Mucosal swelling	Infiltration by neutrophils and monocytes[44]
Enlarged folds	Tumor necrosis factor-alpha gene polymorphism[64]; Genome wide hypomethylation and regional hypermethylation[65,66]; Stimulation of epithelial cell proliferation and inhibition of acid secretion induced by interleukin 1 beta and hepatocyte growth factor[61,62]; Inhibition of acid secretion caused by morphological changes in parietal cells[63]
Xanthoma	Unclear
Atrophy	Cellular injury inflicted by Helicobacter pylori or mediated by inflammation or apoptosis[77]; Th1 immune response[78]; C-X-C motif chemokine receptor 2-mediated cellular senescence[79]
Intestinal metaplasia	Death of parietal cells and reprograming of chief cells[82]

Table 2 Intestinal metaplasia with different mucin secretion

Cells	Incomplete intestinal metaplasia		Complete intestinal metaplasia
	Small intestinal type	Colonic type	Small intestinal type	Colonic type
Columnar cells	Neutral and scanty sialomucins	Sulpho- and scanty sialomucins	No mucin secretion	No mucin secretion
Goblet cells	Sialomucins	sialomucins	Neutral and sialomucins	Sulpho- and sialomucins