ABSTRACT
Background:It has been demonstrated that acid secretion-related gastric fundic structures do not degenerate in elderly individuals. As specimens obtained from human body are greatly influenced by environmental factors,the results need to be further verified by standard animals. Aims:To investigate the aging-related changes of histology of gastric fundus and ultrastructure of fundic gland in beagle dogs. Methods:Nineteen healthy beagle dogs were divided into three age groups,8 in younger group(aged 1-5 years),5 in junior elderly group(aged 6-8 years)and 6 in senior elderly group (aged ≥9 years). Gastric specimens obtained from the fundus were examined by light microscope,the thickness of lamina propria and percentage of parenchymal area of fundic gland in lamina propria were measured,and the parietal cells,chief cells and endocrine cells were counted. Ultrastructure of fundic gland cells were observed by electron microscopy,and the area percentages of related organelles were calculated. Results:The thickness of lamina propria in gastric fundus of beagle dogs showed a decline tendency with aging,but no significant differences were found among the three age groups(P >0. 05);in senior elderly group,a marked decrease in density of fundic gland was observed and with an increase of interstitial tissues. The amount of parietal cells and the area percentages of mitochondria and tubulovesicle in parietal cells showed no aging-related reduction(P > 0. 05),while the amount of chief cells,area percentages of zymogen granule in chief cells,and mucous granule in mucous neck cells were significantly decreased in senior elderly group(P < 0. 05). The amount of endocrine cells increased gradually with aging(P < 0. 05). Conclusions:Aging-related degeneration is not existed in acid secretion-related parietal cells and organelles in gastric fundus of beagle dogs. Furthermore,endocrine cells which secret histamine,gastrin,and somatostatin,etc. for stimulating acid secretion even increased. These changes might be a compensatory mechanism for acid secretion in elderly individuals.
ABSTRACT
Objective To discuss the possible enteric nervous pathogenesis in gastritis related GI motor disorders on the expression changes of protein gene product9. 5 in neurons from the gastric walls of gastritis rat model. Methods 35 clean grade Wister rats were randomly divided into 3 groups, which included gastritis group A (n =10), gastritis group B(n =15) and control group(n =10). Rats in gastritis group A and B received gastric perfusion of HP and the mixture of 2% aspirin and 0. 6N hydrochloric acid respectively. The control group only received gastric perfusion of saline. All of the rats were killed and the gastric mucosal tissues were obtained for the pathological and HP examination. After immunohistochemical pretreatment, the tissues were stained with PGP9. 5 and at the same time the maximum diameter (Dmax, μm), mean area(μm2) and mean optical density (nm) of the neurons from the gastric walls were compared among the groups with Image-Pro Plus professional image analysis system. Results In gastric group A, HP could be found sparsely in the mucous layer or gastric pits, and all of the rapid urease tests were positive. In the other two groups, HP could not be found, and all of the rapid urease tests were negarive. In both gastric group A and B, different grades of inflammatory cell infiltration with active inflammation signs could be found in the deep layers of mucosa, while the control group was normal. The expression mean area, mean optical density of neurons from the gastric wall of rat in group A[(77. 10 ±48. 46) μm2, (53. 25 ±41.40) nm] or B [(73. 92 ± 39. 60) μm2, (45.33 ± 33.20) nm] was obvious lower than control group [(143.51 ± 29. 84) μm2, (85. 00 ± 14. 32) nm], while there was no significant difference between gastric group A and B (P ＞0. 05) (table 1). Conclusions Hp and NSAIDs might cause gastritis and decrease the PGP9. 5 expression of Neurous from gastric walls. The decrease of PGP9. 5 expression of neurons from the gastric wall might contribute to the pathogenesis of GI motor disorders or symptoms of functional dyspepsia.
ABSTRACT
Objective To explore the effects of H.pylori and crude extracted proteins secreted by H.pylori(broth culture filtrate protein,BCF-P)on acid secretion from isolated rabbit parietal cells.Methods Parietal cells from rabbit gastric mucosa were isolated and enriched with digestion and elutriation.H.pylori(NCTC 11637,CagA+ VacA+)were grown in liquid broth culture and BCF-P was precipitated with ammonium sulfate.The vacuolation activity of BCF-P was evaluated with neutral red dye uptake test in HeLa cell.Isolated parietal cells were incubated with H.pylori(bacteria/cell=100∶1)for 2 h and 16 h,or BCF-P(100μg/ml)for 1 h and 12 h.Acid secretion from parietal cells was studied using 14C-aminopyrine(14C-AP)accumulation indirectly and H+-K+ ATPase α subunit mRNA expression was assessed using RT-PCR.Results (1)BCF-P containing vacuolating cytotoxin(VacA)with vacuolation activity on HeLa cells had positive result on neutral red uptake test.(2)The basal expression of H+-K+ ATPase α subunit mRNA could be detected in isolated parietal cells and 14C-AP accumulation was significantly increased in response to the stimulation of histamine with different concentrations for 30 min(P＜0.05).These results indicated that the isolated parietal cells retain relative intact acid secretion function.(3)The histamine(1.0×104 mol/L)stimulated acid secretion was inhibited sustainedly in response to H.pylori by 81% at 2 h and by 94% at 16 h(P＜0.05).However,H+-K+ ATPase α subunit mRNA expression was up-regulated in tlle acute period(2 h)and was down-regulated in the chronic period (16 h)by H.pylori(P＜0.05).(4)BCF-P significantly inhibited the histamine-stimulated acid secretion by 24% at 1 h and by 58% at 12 h(P＜0.05),and this inhibition was accompanied by the down-regulated expression of H+-K+ATPase α subunit mRNA.Conclusions Intact H.pylori and VacA secreted by H.pylori could directly inhibit histamine-stimulated acid secretion from parietal cells and this inhibition may be mediated by the down-regulated H+-K+ ATPase expression.
ABSTRACT
The aims of this study were to evaluate the clinicopathologic features of Helicobacter heilmannii-associated gastritis and to compare H. heilmannii-associated gastritis with H. pylori-associated gastritis. We reviewed 5,985 consecutive gastric biopsy specimens. All cases of chronic gastritis with Helicobacter infection were evaluated with the Updated Sydney System, and the grades of all gastritis variables were compared between H. heilmannii-associated gastritis and H. pylori-associated gastritis groups. There were 10 cases of H. heilmannii-associated gastritis (0.17%) and 3,285 cases of H. pylori-associated gastritis (54.9%). The organisms were superficially located within the mucous layer without adhesion to epithelial cells. Interestingly, in one case many intracytoplasmic H. heilmannii organisms were observed in parietal cells with cell damage. A case of low-grade mucosa-associated lymphoid tissue (MALT) lymphoma concomitant with H. heilmannii infection was detected. Compared to H. pylori-associated gastritis, H. heilmannii-associated gastritis showed less severe neutrophilic activity (p<0.0001), mononuclear cell infiltration (p=0.0029), and endoscopic findings of chronic gastritis devoid of erosion or ulcer (p=0.0309). In conclusion, we present the detailed clinicopathologic findings of H. heilmanniiassociated gastritis compared to H. pylori-associated gastritis. H. heilmannii-associated gastritis is uncommon and milder than H. pylori-associated gastritis, however it may be noteworthy with respect to the development of MALT lymphoma.
Subject(s)
Middle Aged , Male , Humans , Female , Adult , Stomach Neoplasms/etiology , Lymphoma, B-Cell, Marginal Zone/etiology , Helicobacter pylori , Helicobacter heilmannii , Helicobacter Infections/pathology , Gastritis/pathologyABSTRACT
Isolation of rat gastric mucosal cells was performed with scraping method followed by protease and collagenase digestion. Parietal cells were observed and identified with phase-contrast microscopy, light microscopy with hematoxylin and eosin staining, electron microscopy, fluorescence microscopy, and also immunocytochemistry technique. The diameters of parietal cells were measured. The results showed that the mucosal cells were successfully isolated, and it was confirmed that the parietal cells were the biggest cells among all the mucosal cells.