Figure 6 Immunostaining of muramidase and of CD68 (hAR polymer method, 10 magnification). a) Muramidase in the mostly normal mucosa. Muramidase was noted in glandular cells from the surface to the neck portion. b) Muramidase in inflamed mucosa. Muramidase was also noted in deep fundic glandular cells. c) CD68 in an area of intestinal metaplasia. There were CD68 positive cells in the stroma and CD68 positive metaplastic glandular cells..
Homeostatic Mass Control in Gastric Non Neoplastic Epithelia under Infection of Helicobacter pylori: An Immunohistochemical Analysis of Cell Growth, Stem Cells and Programmed Cell Death
Acta Histochem Cytochem. 2008 Jun 27; 41(3):23-38
We evaluated homeostatic mass control in non neoplastic gastric epithelia under Helicobacter pylori (HP) infection in the macroscopically normal appea.....
We evaluated homeostatic mass control in non neoplastic gastric epithelia under Helicobacter pylori (HP) infection in the macroscopically normal appearing mucosa resected from the stomach with gastric cancer, immunohistochemically analyzing the proliferation, kinetics of stem cells and programmed cell death occurring in them. Ki67 antigen positive proliferating cells were found dominantly in the elongated neck portion, sparsely in the fundic areas and sporadically in the stroma with chronic infiltrates. CD117 could monitor the kinetics of gastric stem cells and showed its expression in two stages of gastric epithelial differentiation, namely, in transient cells from the gastric epithelial stem cells to the foveolar and glandular cells in the neck portion and in what are apparently progenitor cells from the gastric stem cells in the stroma among the infiltrates. Most of the nuclei were positive for ssDNA in the almost normal mucosa, suggesting DNA damage. Cleaved caspase 3 positive foveolar cells were noted under the surface, suggesting the suppression of apoptosis in the surface foveolar cells. Besides such apoptosis of the foveolar cells, in the severely inflamed mucosa apoptotic cells were found in the neck portion where most of the cells were Ki67 antigen positive proliferating cells. Beclin 1 was recognized in the cytoplasm and in a few nuclei of the fundic glandular cells, suggesting their autophagic cell death and mutated beclin 1 in the nuclei. Taken together, the direct and indirect effects of HP infection on the gastric epithelial proliferation, differentiation and programmed cell death suggested the in situ occurrence of gastric cancer under HP infection.
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