Cell loss from human gastric mucosa measured by the estimation of deoxyribonucleic acid (DNA) in gastric washings.

Croft, D N; Pollock, D. J.; Coghill, N. F.

doi:10.1136/gut.7.4.333

Cited by 80 publications

(41 citation statements)

References 44 publications

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“…Other studies performed by Croft et al (1966) and Castrup (1977) show that the cell cycle becomes There is a higher binding of tritiated actinomycin in euchromatin (derepressed) than in heterochromatin (repressed) (Berlowitz et al, 1969). In agreement with this view, we have demonstrated (Stoffels et al, 1972) that intestinal metaplasia is not a homogeneous change.…”

Section: Atrophic Mucosasupporting

confidence: 89%

Nuclear binding of tritiated actinomycin in surface epithelial cells from normal stomach and atrophic gastritis.

Stoffels¹,

Preumont²,

Reuck³

1978

Gut

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(Schindler, 1965; Siurala etal., 1966;Walker et al., 1971). Numerous authors have investigated cell proliferation kinetics in normal and atrophic stomach mucosa. An increased proliferation of the epithelial cells in the latter has been described (Deschner and Lipkin, 1976), while in cases of intestinalisation of the gastric mucosa, which is found in over 90% of gastric cancers (Morson, 1959), the same authors have described an impairment of epithelial cell maturation.Earlier work has reported an increased nuclear fixation of tritiated actinomycin (3H-AM) in cancer cells as compared to the corresponding normal cells Pileri et al., 1972;Heenen et al., 1973). This technique has been shown to be a valid method for the rough evaluation of the number of free DNA sites: the fixation of labelled actinomycin by the nuclei is closely linked to the degree of repression in chromatin (Brachet and Ficq, 1965;Brachet, 1971).'Address for correspondence: Dr G. Stoffels, H6pital Universitaire Brugmann, 4, Place Van Gehuchten, 1020 Bruxelles.Received for publication 4 May 1978 In this study, we have compared the binding of 3H-AM to chromatin in epithelial cells in normal stomachs and in atrophic gastritis by autoradiographs. Significant increases of 3H-AM binding would suggest that these cells are in a depressed state. MethodsTwenty-five patients were studied; eight had a normal gastric mucosa and 17 had a atrophic gastritis as defined by the histological criteria described by Whitehead et al. (1972).The grades of gastritis were (1) superficial, and (2) atrophic with three grades: mild, moderate, and severe. Superficial gastritis is characterised by mononuclear and polymorphonuclear cell infiltration located in the surface epithelium and gastric pit region. In mild atrophic gastritis the infiltration occurs into all layers of lamina propria with a slight reduction of parietal and chief cells. Moderate and severe atrophic gastritis includes all the above signs, in addition to a greater reduction in parietal and chief cells, and the presence of intestinal metaplasia and regenerative nodules.It must be remembered that in this classification 'active atrophic gastritis' signifies the presence of 870 on 25 March 2019 by guest. Protected by copyright.

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Section: Atrophic Mucosasupporting

confidence: 89%

Nuclear binding of tritiated actinomycin in surface epithelial cells from normal stomach and atrophic gastritis.

Stoffels¹,

Preumont²,

Reuck³

1978

Gut

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“…The human gastric epithelium is renewed continuously throughout life with an estimated 500,000 cells shed/min in adults (1). Dysregulated renewal results in a number of disease states including gastric adenocarcinoma, the second most common cause of cancer-related deaths worldwide (2).…”

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confidence: 99%

Molecular Characterization of Mouse Gastric Zymogenic Cells

Mills

Andersson

Stappenbeck

et al. 2003

Journal of Biological Chemistry

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“…While no studies have been conducted to date measuring free purines in the gastric mucus, numerous studies have been conducted showing large quantities of extracellular DNA present in the mucus layer due largely to epithelial cell turnover (23,24). These DNA concentrations were at one time used to show epithelial cell turnover rates, and it was found that patients diagnosed with gastritis have larger average amounts of DNA in their gastric mucus, as measured by gastric rinsings (23).…”

Section: Discussionmentioning

confidence: 99%

“…The level of DNA present in the mucus layer of the human stomach is substantial (23,24) and could prove to be an important source of purines for this pathogenic bacterial auxotroph. The ability to utilize extracellular DNA is present in many environmental bacteria (25,26), as well as in bacterial pathogens (27).…”

mentioning

confidence: 99%

Helicobacter pylori Salvages Purines from Extracellular Host Cell DNA Utilizing the Outer Membrane-Associated Nuclease NucT

Liechti

Goldberg

2013

J Bacteriol

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Helicobacter pylori is a bacterial pathogen that establishes life-long infections in humans, and its presence in the gastric epithelium is strongly associated with gastritis, peptic ulcer disease, and gastric cancer. Having evolved in this specific gastric niche for hundreds of thousands of years, this microbe has become dependent on its human host. Bioinformatic analysis reveals that H. pylori has lost several genes involved in the de novo synthesis of purine nucleotides, and without this pathway present, H. pylori must salvage purines from its environment in order to grow. While the presence and abundance of free purines in various mammalian tissues has been loosely quantified, the concentration of purines present within the gastric mucosa remains unknown. There is evidence, however, that a significant amount of extracellular DNA is present in the human gastric mucosal layer as a result of epithelial cell turnover, and this DNA has the potential to serve as an adequate purine source for gastric purine auxotrophs. In this study, we characterize the ability of H. pylori to grow utilizing only DNA as a purine source. We show that this ability is independent of the ComB DNA uptake system, and that H. pylori utilization of DNA as a purine source is largely influenced by the presence of an outer membrane-associated nuclease (NucT). A ⌬nucT mutant exhibits significantly reduced extracellular nuclease activity and is deficient in growth when DNA is provided as the sole purine source in laboratory growth media. These growth defects are also evident when this nuclease mutant is grown in the presence of AGS cells or in purine-free tissue culture medium that has been conditioned by AGS cells in the absence of fetal bovine serum. Taken together, these results indicate that the salvage of purines from exogenous host cell DNA plays an important role in allowing H. pylori to meet its purine requirements for growth.

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Cell loss from human gastric mucosa measured by the estimation of deoxyribonucleic acid (DNA) in gastric washings.

Cited by 80 publications

References 44 publications

Nuclear binding of tritiated actinomycin in surface epithelial cells from normal stomach and atrophic gastritis.

Nuclear binding of tritiated actinomycin in surface epithelial cells from normal stomach and atrophic gastritis.

Molecular Characterization of Mouse Gastric Zymogenic Cells

Helicobacter pylori Salvages Purines from Extracellular Host Cell DNA Utilizing the Outer Membrane-Associated Nuclease NucT

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