Human Gastric Biopsy Specimens Research Articles

Demonstration of a phospholipid-rich zone in the human gastric epithelium damaged by Helicobacter pylori

Background: Recently, a hydrophobic layer has been shown by the contact angle method in human gastric biopsy specimens. The aim of this study was to show the existence of a phospholipid-rich layer in the human gastric epithelium and to investigate the influence of Helicobacter pylori on these structures. Methods: Biopsy specimens from the gastric antrum were obtained during gastroscopy from patients with normal gastric mucosa as well as from patients with H. pyloripositive gastritis for electron microscopical and histological examination. Structures reacting with a phospholipid-selective stain, iodoplatinate were analyzed by electron microscopy and electron-dispersive x-ray microanalysis. Results: Both methods revealed the morphological existence of a phospholipid-rich zone covering the human gastric epithelial layer. Reaction products could be localized within the cells, at the epithelium closely associated with the surface, and in connection with the mucus. In infected tissue, H. pylori affects iodoplatinate-reactive material within the mucous layer and material covering the epithelium. Conclusions: The phospholipid-rich zone in the apical region of surface mucous cells is likely to represent an important factor of the gastric protective system in humans. The destruction of this hydrophobic layer may result in a reduction of hydrophobicity giving access to gastric acid.

Adhesion ofHelicobacter pylorito Human Gastric Mucosal Biopsy Specimens Cultivated in Vitro

The therapeutic advances in Helicobacter pylori infection is hampered by the lack of suitable animal model systems. We have previously reported on successful adherence of H. pylori to pig gastric mucosa cultured in vitro. The aim of this study was to verify the technique in human biopsy specimens cultured in vitro. Mucosal samples were taken from H. pylori-negative and H. pylori-positive patients undergoing gastric surgery. The non-infected tissue was infected with H. pylori in vitro, and the infected tissue was put into culture immediately. Total number and those H. pylori firmly attached were checked throughout a 72-h culture. Viability of cultured human gastric mucosa was good and unaffected by the presence of H. pylori. The amount of bacteria adhering, increased with time from 0.01% to 2-4% after 72 h in culture. In vivo-infected specimens initially had a low number of firmly attached H. pylori, but total H. pylori increased with time in culture. It is concluded that human gastric biopsy specimens show good viability for 72 h and that viability and cell division of H. pylori were maintained in both in vivo and in vitro H. pylori-infected tissue. In both cases the total number of viable bacteria attached to the specimens increased with incubation time.

Immunoassay of Pig and Human Gastric Proton Pump

Monoclonal antibodies against the K+-dependent adenosine triphosphatase (ATPase) responsible for acid secretion in the pig gastric mucosa were generated by hybridoma technology. Two of these antibodies, shown to bind selectively to subunits of the ATPase and to label intracellular membranes of pig and rabbit parietal cells, were used to develop a sensitive (less than 1 pmol) immunoassay for the ATPase. Enzyme samples were adsorbed to the wells of polystyrene microtitration plates and then incubated sequentially with monoclonal antibody, antimouse immunoglobulin G coupled to alkaline phosphatase, and p-nitrophenyl phosphate. Standard curves relating the absorbance of the wells at 410 nm to log10 micrograms ATPase were fitted by a three-parameter logistic, with a useful assay range of 0.05-10 micrograms ATPase. The immunoassay allows measurement of proton-pumping ATPase levels in human gastric biopsy specimens and may therefore be useful in studies of gastric mucosal function.

Human gastric mucosal adenylate cyclase activity: effects of various cytoprotective prostaglandins.

Several prostaglandins prevent ulcer formation (called cytoprotection) by a mechanism other than inhibition of gastric acid secretion. One suggestion is that they increase cyclic AMP in non-parietal cells. A variety of prostaglandins with potent cytoprotective properties were tested for their capacity to modulate adenylate cyclase activity in homogenates of human gastric mucosa. Prostaglandin E2, prostacyclin (PGI2) and 15(S)-methyl-PGE2 stimulated the cyclase in human gastric mucosal biopsy specimens in a dose-dependent manner. Cytoprotective prostaglandins without antisecretory properties such as PGF2 beta were also able to activate the enzyme system dose-dependently. In contrast, cytoprotective prostaglandins such as PGD2, the PGE1-analogue, SC-29333, and the prostaglandin-like compound C83 did not stimulate human gastric adenylate cyclase. Whereas PGD2 did not modulate enzyme activity at all, SC-29333 and C83, at concentrations greater than 10 mumol/l, inhibited basal and PGE2-stimulated enzyme activities. These studies suggest that cyclic AMP is not directly related to the cytoprotective effect of prostaglandins, at least in human gastric mucosa.

Enzyme histochemical studies of human gastric and jejunal biopsy specimens in normal and disease states

The alkaline phosphatase activity of 28 gastric and 32 jejunal biopsy specimens examined histochemically revealed the following: (1) absence of alkaline phosphatase activity in normal gastric mucosa and in mucosa with varying degrees of gastritis unassociated with intestinal metaplasia; (2) marked alkaline phosphatase activity in the brush border region of the metaplastic cells in 3 patients with gastritis associated with intestinal metaplasia; and (3) no significant difference in alkaline phosphatase activity between the jejunal biopsy specimens of normal patients and those with primary malabsorption syndrome.