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neurons mediate protective vasodilatation in rat gastric mucosa. Am. J. Physiol., 1991, 260 , G363–G370. Saria A. Sensory neurons mediate protective vasodilatation in rat gastric
The aim of the present study was to investigate the expression pattern of claudin-1, -2, -3, -4, -5, -7, -8, -10 and -18 in the intact fundic and pyloric gastric mucosa of dogs. Intense, linear, membranous claudin-18 positivity was detected in the surface gastric cells and in the epithelial cells of the gastric glands both in the fundic and pyloric stomach regions. The mucous neck cells in the apical part of the glands, furthermore the parietal cells and chief cells of the basal part of the gland were all positive for claudin-18, in the same way as the enteroendocrine cells. Cells of the basal part of the pyloric glands showed intense, linear, membranous claudin-2 positivity, but cells of the superficial portion of these glands and the surface gastric cells in this region were claudin-2 negative. Fibroblasts, endothelial cells, lymphocytes of the propria layer, smooth muscle cells and vegetative neurons were all negative for claudin-2. All gastric epithelial cells were negative for claudin-1, -3, -4, -5, -6, -7, -8 and -10. The endothelial cells of the propria layer had intense claudin-5 positivity. We assume that claudin-18 forms a paracellular barrier against gastric acid in the healthy canine stomach, in the same way as in mice.
Gastric ulcer, a major gastrointestinal disorder is currently being treated by drugs which may come with side effects in a long run. Dietary intake of foods may alleviate or prevent gastric ulcer. This study was carried out by pretreating Sprague-Dawley rats with methanolic extracts of soya beans, soya beans fermented with Schizophyllum commune (a common medicinal-edible mushroom), cimetidine (positive control) and 10% Tween 20 (negative control) to evaluate protective effects against ethanol-induced injury in the gastric mucosa. Rats of negative control group showed haemorrhaging in gastric mucosa and were markedly alleviated in rats pretreated with soya bean extracts and cimetidine. When ulceration area was analysed, unfermented and fermented soya bean extracts and cimetidine were significantly better in the protection of the gastric mucosa against ethanol-induced injury compared to the negative control. However, no significant difference was found between pretreatment of both soya bean extracts and cimetidine. In terms of acidity of gastric mucosa content, rats pretreated with fermented soya beans were significantly acidic; whereas the mucus weight was significantly higher in gastric mucosa of rats pretreated with unfermented soya beans. Histological examination of gastric mucosa walls found that rats of the negative control group showed lesions in the mucosa area, oedema and leukocytes infiltration in the submucosa area, and that these were distinctly decreased in gastric mucosa tissue samples of rats pretreated with soya bean extracts and cimetidine; whereby fermented soya beans had a comparable effect with cimetidine. The study shows that S. commune fermented soya beans offer protection against ethanol-induced gastric ulcers in rats.
Solcia, E., Fiocca, R., Villani, L., et al.: Hyperplastic, dysplastic, and neoplastic enterochromaffin-like-cell proliferations of the gastric mucosa. Classification and histogenesis. Am. J. Surg. Pathol., 1995, 19 (Suppl. 1) , S1–S7
A postweaning pig died in spite of antibiotic therapy showing wasting in a small herd. Postweaning multisystemic wasting syndrome (PMWS) was diagnosed on the basis of gross pathological and histological lesions and the presence of moderate amounts of porcine circovirus 2 (PCV2) antigen in tissue samples. Mycotic gastritis caused by Zygomycetes spp. was found on round areas with a diameter of 1 to 3 cm in the glandular mucosa of the stomach. Moderate amount of PCV2 viral antigen was detected almost evently in the stomach and mostly in the macrophages. In addition, acute uraemia, revealed by an ammonia-like stink of the gastric mucosa and the presence of acute erosions on the glandular mucosa of the stomach, was observed as a consequence of PCV2-induced interstitial nephritis. Only PCV2 infection could be identified as a cause of secondary mycotic gastritis. The results further support the immunosuppressive ability of PCV2 infection in PMWS-affected pigs.
Increasing resistance to drugs represents a serious problem in treatment of infections with Helicobacter pylori, providing cause of frequent therapeutic failures. Present study aimed at analysis of changes in resistance of H. pylori to antibiotics in West Poland within the recent 15 years. 108 strains of H. pylori were analysed, isolated from gastric mucosa of adult patients. Group 1 involved 66 strains isolated in years of 1998/1999. Group 2 comprised 42 isolates obtained in years of 2013/2014. Susceptibility to amoxicillin (AMX), clarithromycin (CL), tetracycline (TC) and metronidazole (MTZ) was determined by E-test (AB Biodisc). All strains on both studied groups were susceptible to AMX. In group 1 all strains proved to be susceptible to TC, while 9% and 36% of tested strains were resistant to CL and MTZ, respectively. By contrast, in group 2, 31% and 83% of strains were resistant to CL and MTZ, respectively. In parallel, 14% strains were found to be resistant to TC (according to EUCAST interpretations). In West Poland, within recent 15 years a dramatic increase was noted in H. pylori strains resistant to metronidazole. In parallel, a significant increase was noted in proportion of strains resistant to clarithromycin.
It is well documented that the double-stranded DNA (dsDNA) genomes of certain viruses and the proviral genomes of retroviruses are regularly targeted by epigenetic regulatory mechanisms (DNA methylation, histone modifications, binding of regulatory proteins) in infected cells. In parallel, proteins encoded by viral genomes may affect the activity of a set of cellular promoters by interacting with the very same epigenetic regulatory machinery. This may result in epigenetic dysregulation and subsequent cellular dysfunctions that may manifest in or contribute to the development of pathological changes (e.g. initiation and progression of malignant neoplasms; immunodeficiency). Bacteria infecting mammals may cause diseases in a similar manner, by causing hypermethylation of key cellular promoters at CpG dinucleotides (promoter silencing, e.g. by Campylobacter rectus in the placenta or by Helicobacter pylori in gastric mucosa). I suggest that in addition to viruses and bacteria, other microparasites (protozoa) as well as macroparasites (helminths, arthropods, fungi) may induce pathological changes by epigenetic reprogramming of host cells they are interacting with. Elucidation of the epigenetic consequences of microbe-host interactions (the emerging new field of patho-epigenetics) may have important therapeutic implications because epigenetic processes can be reverted and elimination of microbes inducing patho-epigenetic changes may prevent disease development.
Interleukin-8 (IL-8) is a potent neutrophil-activating chemokine which triggers the infiltration and migration of neutrophils into areas of bacterial infection. Helicobacter pylori-infected patient studies as well as animal models have revealed that H. pylori type I strains carrying an intact cytotoxin-associated gene pathogenicity island (cag-PAI) with a functional type IV secretion system (T4SS) induce IL-8 expression and secretion in gastric mucosa. This gastric mucosal IL-8 expression correlates with severe histological changes due to H. pylori infection.
In the present study, we explored a new recognition pattern on the bacterial adhesion protein CagL inducing IL-8 expression in H. pylori-infected host cells. To analyze the secreted IL-8 concentration, we performed IL-8 enzyme-linked immunosorbent assay (ELISA). To investigate the H. pylori-induced IL-8 expression on the transcriptional level, we transiently transfected gastric epithelial cells (AGS) with a human IL-8 luciferase reporter construct.
The results of this study demonstrate that specifically the C-terminal coiled-coil region of the H. pylori CagL protein, a protein described to be located on the tip of the T4SS-pilus, is responsible for several in vitro observations: 1) H. pylori-induced IL-8 secretion via the transforming growth factor (TGF)-α activated epidermal growth factor-receptor (EGF-R) signaling pathway; 2) H. pylori-induced elongation of the cells, a typical CagA-induced phenotype; and 3) the bridging of the T4SS to its human target cells. This novel bacterial-host recognition sequence allows a new insight into how H. pylori induces the inflammatory response in gastric epithelial cells and facilitates the development of precancerous conditions.
Sanduleanu, S., Jonkers, D., de Bruïne, A., et al.: Changes in gastric mucosa and luminal environment during acid-suppressive therapy: a review in depth. Dig. Liver Dis., 2001, 33 , 707–719. Bruïne A
280 Zhou, L., Sung, J. J., Lin, S. et al.: A five-year follow-up study on the pathological changes of gastric mucosa after H. pylori eradication. Chin. Med. J., 2003
