Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001511 (Adhesion)
 5,955 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Helicobacter pylori is a human pathogen associated with gastritis and peptic ulcer. Adhesion properties of H. pylori to various structures have been described in the literature, including evidence for sialic acid-binding. To study the specificity and frequency of sialic acid-binding, fourteen H. pylori strains were investigated using haemagglutination with derivatized erythrocytes carrying sialic acids only on defined glycans and using haemagglutination inhibition assays. From these studies H. pylori strains can be grouped into sialic acid-dependent and sialic acid-independent classes. The sialic acid-dependent strains require alpha-2,3-linked sialic acid for haemagglutination. The potential roles of sialic acid-dependent adhesions for H. pylori-related infections are discussed.
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PMID:Adhesion of Helicobacter pylori strains to alpha-2,3-linked sialic acids. 898 Oct 92

The aim was to determine the prevalence of Helicobacter heilmannii-like organisms in human gastric biopsies and the associated histology compared with that of Helicobacter pylori-bearing gastric biopsies. Furthermore, the feasibility of culturing H. heilmannii was examined. A consecutive series of 727 gastric biopsies from 650 patients were prospectively scrutinized for H. heilmannii. Their distribution pattern was recorded as well as the affiliated morphology of the gastric mucosa. Additional biopsies from some of the patients were examined microbiologically. Four cases (0.6%)(95% confidence intervals: 0.01-1.2%) of the examined material harboured H. heilmannii. The bacterial burden was graded as sparse in three cases, moderate in one case. The distribution pattern was patchy; thus, in no case did all biopsies from one endoscopy comprise H. heilmannii. Adhesion to epithelial cells was infrequent. A mild gastritis, active in three cases, characterized all biopsies. Lymphoid aggregates occurred in biopsies from three patients. Micropapillary tufting of the epithelial layer and intestinal metaplasia were not apparent. Culture studies proved successful in the one of the four cases assayed. In conclusion the morphology of H. heilmannii-bearing mucosa deviates from that of H. pylori-associated mucosa by the absence of epithelial damage in the former. This observation can in part be explained by the predominant location of H. heilmannii at a distance from the epithelium in contrast to the conspicuous H. pylori adhesion to epithelial cells, coupled with a usually low bacterial burden and patchy occurrence of H. heilmannii as opposed to the generally more heavy infestation with H. pylori.
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PMID:The histopathology of human gastric mucosa inhabited by Helicobacter heilmannii-like (Gastrospirillum hominis) organisms, including the first culturable case. 936 89

Helicobacter pylori infection of the stomach results in acute inflammation followed by chronic inflammation, but the mechanism is unknown. Adhesion molecules such as ICAM-1, Mac-1, and LFA-1 may help regulate interactions of immune cells and inflammatory cells. We used immunohistochemistry to locate these molecules in the gastric mucosa of patients with chronic gastritis arising from H. pylori infection. Biopsy specimens were taken from five H. pylori-negative healthy volunteers and 20 H. pylori-positive patients with chronic gastritis for immunohistochemical studies of adhesion molecules. In the gastric mucosa of patients with H. pylori-associated chronic gastritis, ICAM-1 expression was prominent in most of the vessels and inflammatory cells, such as lymphocytes and granulocytes, in the lamina propria. However, no intraepithelial lymphocytes and surface epithelial cells expressed ICAM-1. Antigen-presenting cells (APCs), such as macrophages, expressed ICAM-1 as well as HLA-DR antigen. LFA-1 and Mac-1 were strongly expressed in these immune and inflammatory cells. The number of vascular endothelial cells positive for P-selectin was also greater in H. pylori-positive mucosa. The expression of these molecules decreased remarkably after successful eradication of H. pylori. In conclusion, ICAM-1 is the predominant form among the cell adhesion molecules that are expressed in response to chronic H. pylori infection. The increased expression of ICAM-1 is linked with massive infiltration of inflammatory cells that express LFA-1 and Mac-1, and also with APCs that express HLA-DR, suggesting that ICAM-1 exerts a key role in immuno-inflammatory responses in gastric mucosa of patients with H. pylori-associated gastritis.
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PMID:In situ expression of cell adhesion molecules in chronic gastritis with Helicobacter pylori infection. 947 51

Adhesion molecules and cytokines are known to be involved in the formation of acute gastric mucosal injury. However, it is not clear whether the gastric mucosal cells express these molecules and modulate the inflammation. To clarify whether gastric mucosal cells express intercellular adhesion molecule-1 (ICAM-1) and proinflammatory cytokines (tumor necrosis factor-alpha (TNF-alpha), interleukin-1-alpha (IL-1-alpha), and cytokine-induced neutrophil chemoattractant-2-beta (CINC-2-beta)) in the formation of gastric mucosal injury, we have used rat indomethacin-induced gastric mucosal lesions as an in vivo model. The gene expression of all cytokines and ICAM-1 increases at the early stages of indomethacin-induced gastritis (TNF-alpha and IL-1-alpha gene expression began to increase earlier than that of ICAM-1 and CINC-2-beta) and can mainly be detected in the gastric epithelial layer. To further identify the source of those molecules, the epithelial cells were separated into seven fractions according to their sizes by a counterflow elution. ICAM-1 and CINC-2-beta gene expressions are particularly enhanced in the middle-sized cell fractions that are rich in gastric mucous-producing cells. The effect of TNF-alpha or IL-1-alpha on the gene expression of ICAM-1 and cytokines was examined by using RGM-1 cells as a model for gastric mucosal cells. RGM-1 cells show an augmented ICAM-1 and proinflammatory cytokine expression in response to TNF-alpha or IL-1-alpha stimulation. Moreover, immunohistochemical staining also reveals an increase in ICAM-1 and CINC protein production in RGM-1 cells in response to TNF-alpha stimulation. We conclude that gastric mucosal cells express various cytokines and an adhesion molecule during the formation of acute gastric mucosal injury and that they may modulate the inflammation.
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PMID:Rat gastric mucosal cells express ICAM-1 and proinflammatory cytokines during indomethacin-induced mucosal injury. 962 89

Reactive oxygen metabolites play an important role in the pathogenesis of gastroduodenal mucosal inflammation (mucosal ischemic injury and other models of mucosal damage induced by nonsteroidal anti-inflammatory drugs, ethanol, or H. pylori), peptic ulcer disease, and gastric cancer. H. pylori achieves its pathogenetic role by triggering an intense leukocyte infiltration of the gastric mucosa, and neutrophil activation provides a major source of reactive oxygen metabolites which can cause tissue damage mainly in the absence of antioxidants. H. pylori virulence factors promote release of a variety of chemoattractants/inflammatory mediators. Circulating leukocytes are recruited to sites of inflammation by a well-regulated and coordinated process that largely occurs in postcapillary venules. Adhesion molecules are expressed on the surface of endothelial cells and leukocytes serve to ensure an orderly sequence of cell-to-cell interactions that sustain leukocyte adherence to vascular endothelium and the subsequent transendothelial migration into inflamed tissue. Transcriptional factors are involved in the expression of endothelial adhesion molecules, and regulation of activity of these factors (i.e., NF-kappa B) is a very attractive target for therapeutic interventions. Longstanding H. pylori-associated gastritis predisposes to gastric cancer development and reactive oxygen metabolites play a part in H. pylori-related gastric carcinogenesis. Various regimens of reactive oxygen metabolite scavengers appear to be new treatment strategies for upper gastrointestinal diseases.
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PMID:Reactive oxygen metabolites and upper gastrointestinal diseases. 1146 18

Helicobacter pylori infection leads to a broad spectrum of disease manifestations such as gastritis, ulcer disease, and even gastric carcinoma. The genetically determined immune response and subsequent inflammation influence the degree of mucosal damage. Adhesion molecules of the CD11 cluster play an important role in adherence of neutrophils to endothelial cells in inflammation. We conducted a haplotype-based analysis of the CD11 cluster in a sample of 315 patients with H. pylori infection and investigated associations with gastric erosions and ulcer disease. Twelve single nucleotide polymorphisms (SNPs) covering the genes CD11a, CD11b, and CD11c were genotyped by Taqman technology. Linkage disequilibrium (LD) was assessed within the CD11 cluster and haplotype case-control analysis was conducted. Sliding window haplotype analysis identified a haplotype consisting of the markers CD11c exon 15 and intron 31 associated with gastric ulcer disease. Patients carrying the haplotype GA bear a 2.4-fold increased risk. No significant associations of single markers with disease outcome were found. High-density LD mapping and mutation detection of CD11c in larger samples will be necessary to confirm our findings and identify the causative variant. Thus, we conclude that genetic variants in the CD11 cluster may play a role in the development of gastric ulcer in chronic H. pylori infection presumably by influencing leukocyte adhesion. The biological effect of genetic variants of CD11c in gastric inflammation needs further clarification.
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PMID:Haplotype analysis of the CD11 gene cluster in patients with chronic Helicobacter pylori infection and gastric ulcer disease. 1573 May 20

Helicobacter pylori infects more than half of the world's population. Although most patients are asymptomatic, persistent infection may cause chronic gastritis and gastric cancer. Adhesion of the bacteria to the gastric mucosa is a necessary prerequisite for the pathogenesis of H. pylori-related diseases and is mediated by mucin O-glycans. In order to define which glycans may be implicated in the binding of the bacteria to the gastric mucosa in humans, we have characterized the exact pattern of glycosylation of gastric mucins. We have identified that the major component was always a core 2-based glycan carrying two blood group H antigens, whatever was the blood group of individuals. We have also demonstrated that around 80% of O-glycans carried blood group A, B or H antigens, suggesting that the variation of gastric mucin glycosylation between individuals is partly due to the blood group status. This study will help better understanding the role of O-glycans in the physiology and homeostasis of gastric mucosa. Overall, the results reported here give us the necessary background information to begin studies to determine whether individuals who express certain carbohydrate epitopes on specific mucins are predisposed to certain gastric diseases.
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PMID:Almost all human gastric mucin O-glycans harbor blood group A, B or H antigens and are potential binding sites for Helicobacter pylori. 2252 99