Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P10145 (IL-8)
 23,849 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To determine the role of host genetic factors in Helicobacter pylori infection, we examined the relation between gastroduodenal diseases and IL-1B polymorphisms in patients with H. pylori infection. In addition, we also compared gastric mucosal cytokine levels in those patients. We confirmed the findings that the IL-1B-31 C-to-T base transition was inverted in association with the -511 T-to-C base transition. There was no relation regarding to IL-1B polymorphisms and clinical outcomes. The gastric mucosal IL-1B level of the body of the stomach but not the antrum was significantly different among IL-1B genotypes. Furthermore, the IL-8 levels in the body were also higher in IL-1B-511C/C/ IL-1B-31TT than H. pylori negative patients. These findings suggested that IL-1B polymorphisms enhance not only IL-1-B production but also IL-8 production in the gastric body and may play an important role in the development of atrophic gastritis.
 ...
PMID:Cytokine expressions and H. pylori-associated gastric mucosal lesion. 1252 38

H. pylori colonisation of the stomach causes the recruitment of the inflammatory cells by the adherence of the bacteria with the epithelium and the release of factors of virulence either to the contact (oipA or other soluble factors) or in the cell by translocation (CagA). Such contact triggers interleukin 8 expression in the epithelial cell and attracts lymphocytes and monocytes into the chorion. Bacterial lipopolysaccharide and urease support the activation of these inflammatory cells. The lymphocytes produce pro-inflammatory cytokines, which direct the immune response towards the Th1 pathway. The variability of the inflammatory response depends on hereditary factors of the host such as the interleukin 1 genotypes, which determine the level of the pro-inflammatory cytokine expression, and of bacterial factors such as the cag pathogenicity island, the lipopolysaccharide and the vacuolating toxin, vacA. The mucosal inflammation provokes apoptosis and atrophy of the epithelial cells through the effect of pro-inflammatory cytokines and free radicals. Epithelial proliferation is a consequence of excessive apoptosis caused by the infection. It is stimulated by the expression of inducible cyclo-oxygenase and inducible nitric oxide synthase. The development of atrophic gastritis towards cancer is supported by nitric oxide which has a mutagenic effect on DNA and inhibits p53 protein and by the bacterium itself which decreases DNA mismatch repairing activity. The gastritis induced by Helicobacter pylori changes acid secretion according to the prevalent location of the gastritis in the antrum or in the gastric body. Prevalent gastritis in the gastric body causes hypochlorhydria by reducing the release of histamin from ECL cells and inhibiting the parietal cells through the effect of tumor necrosis factor and interleukin 1-beta. Hypochlorhydria is more marked among patients having a pro-inflammatory genotype for interleukin 1-beta and those infected by bacteria with virulence factors. In the event of antrum predominant gastritis, the pro-inflammatory cytokines cause a reduction of somatostatin and gastrin releases from the D and the G cells, respectively. The result of all is increased maximal acid output and the meal-stimulated acid secretion.
 ...
PMID:[What are the gastric modifications induced by acute and chronic Helicobacter pylori infection?]. 1270 Apr 95

Helicobacter pylori(H. pylori) is an important pathogenic factor for gastroduodenal ulcers and gastric cancer. The level of gastric acid output may influence the outcome of those diseases. With low acid output, H. pylori can spread to the corpus of the stomach, resulting in progression to atrophic gastritis. It may cause an increased risk of gastric cancer and ulcer. In contrast, with high output, H. pylori is confined in the gastric antrum, which develops antrum-predominant gastritis. This may contribute to an increased risk of duodenal ulcer. It is well known that inflammatory cytokines including interleukin (IL)-1 beta, IL-8 and tumor necrosis factor alpha modulate gastric acid secretion. Therefore, the host immune response by the cytokines may cause these disparate pathways in gastric acid secretion.
 ...
PMID:[Helicobacter pylori-related cytokines influence gastric acid secretion and gastric mucosal inflammation in gastroduodenal ulcers]. 1503 84

To determine the role of host immune responses in H. pylori infection, we examined the relationship between gastric mucosal IL-8 levels and histological gastritis in patients with H. pylori infection. Biopsy tissue obtained from 99 patients were homogenizedand mucosal IL-8 levels measured by ELISA. The gastric mucosal IL-8 levels in both the antrum and corpus were higher in patients with H. pylori than in H. pyloi negativepatients. IL-8 levels in the corpus but not the antrum correlated with the severity of the atrophy. The IL-1B polymorphism had no influence on the degree of IL-8 production. These findings indicate that IL-8 production is independent of IL-1B polymorphisms and IL-8 may play an important role in the development of atrophic gastritis.
 ...
PMID:Relationship between gastric mucosal IL-8 levels and histological gastritis in patients with Helicobacter pylori infection. 1614 97

Host genetic susceptibility may influence gastric carcinogenesis caused by Helicobacter pylori infection. We aimed to clarify the relationship of interleukin (IL)-8 polymorphism with the risk of atrophic gastritis and gastric cancer. We examined IL-8 -251 T > A, IL-1B -511 C > T, and IL-1RN intron 2 polymorphisms in 252 healthy controls, 215 individuals with atrophic gastritis, and 396 patients with gastric cancer. We also investigated the effect of the IL-8 polymorphism on IL-8 production and histologic degree of gastritis in noncancerous gastric mucosa. Although no correlation was found in the analysis of the IL-1B and IL-1RN polymorphisms, IL-8 -251 A/A genotype held a higher risk of atrophic gastritis [odds ratio (OR), 2.35; 95% confidence interval (CI), 1.12-4.94] and gastric cancer (OR, 2.22; 95% CI, 1.08-4.56) compared with the T/T genotype. We also found that the A/A genotype increased the risk of upper-third location (OR, 3.66; 95% CI, 1.46-9.17), diffuse (OR, 2.79; 95% CI, 1.21-6.39), poorly differentiated (OR, 2.70; 95% CI, 1.14-6.38), lymph node (OR, 2.50; 95% CI, 1.01-6.20), and liver metastasis (OR, 5.63; 95% CI, 1.06-30.04), and p53-mutated (OR, 1.91; 95% CI, 1.13-3.26) subtypes of gastric cancer. The A/A and A/T genotypes were significantly associated with higher levels of IL-8 protein compared with the T/T genotype. Neutrophil infiltration score was significantly higher in the A/A genotype than in the T/T genotype. In conclusion, we showed that the IL-8 -251 T > A polymorphism is associated with higher expression of IL-8 protein, more severe neutrophil infiltration, and increased risk of atrophic gastritis and gastric cancer.
 ...
PMID:Interleukin-8 promoter polymorphism increases the risk of atrophic gastritis and gastric cancer in Japan. 1628 68

Helicobacter pylori (HP) infection affects over 50% of the world's population. The prevalence is over 90% in populations at high risk for gastric cancer, but clinical outcomes of the infection are highly variable and thus host genetic factors have been suggested to play a role in its outcomes in addition to bacterial factors. In this study, we examined the effects of common functional genetic polymorphisms of several proinflammatory cytokines known to be overexpressed in HP-infected gastric mucosa on the risk of various stages of gastric premalignant lesions. The odds ratios (ORs) and 95% confidence intervals (CI) for atrophic gastritis, intestinal metaplasia and dysplasia were estimated by multinominal logistic regression analysis among 2,033 Venezuelan subjects. There was a significant effect of IL8 -251A allele on the prevalence of dysplasia (p = 0.021). The OR associated with the A-allele was 1.34 (95% CI: 0.82-2.18) for heterozygotes and 2.00 (95% CI: 1.13-3.56) for homozygotes, compared with the TT genotype. Furthermore, there was a statistically significant interaction between the number of A-alleles and HP cag A genotype (p = 0.009), suggesting that the A-allele increased the risk of dysplasia only when cag A was present. The OR for the AA compared with TT genotype was 3.22 (95% CI: 1.60-6.52) in this group. There were no associations with other proinflammatory cytokines studied, i.e., IL1 beta, IL6, monocyte chemoattractant protein 1 (MCP1) and TNF alpha, or with other stages of premalignant lesions. The present study provides important evidence suggesting host-bacterial interactions in the development of gastric precancerous lesions.
 ...
PMID:Host-bacterial interaction in the development of gastric precancerous lesions in a high risk population for gastric cancer in Venezuela. 1667 Oct 87

Although the gastric cancer incidence is decreasing, this neoplasia remains one of the major causes of oncological mortality. Because of an insidious development, gastric cancer is often diagnosed in an advanced stage and consequently with a poor prognosis. Accurate non-invasive tests should be extremely useful in order to detect gastric neoplasm in an early phase. In clinical practice, there is no reliable bio-marker for detecting this malignant disease. However, intestinal as well as diffuse types of gastric cancer are preceded by gastric mucosa inflammation. Furthermore, the intestinal type of the neoplasia is, generally, related to chronic atrophic gastritis, especially if associated with intestinal metaplasia. In particular, the risk of the neoplasm is linked to both extension and severity of gastric atrophy. Serological parameters such as serum pepsinogens I (PGI) and II (PGII), gastrin-17 (G-17) cytokines (e.g. IL-8), antiparietal cells, IgG anti-Hp and CagA antibodies and lastly ghrelin supply information about either atrophic or inflammatory conditions characterising gastric mucosa. Low PGI and PGI/PGII ratio levels, especially if combined with high G-17 levels, are recognised bio-markers of corpus atrophic gastritis. Low G-17 levels could be, also, suggestive of antral atrophic gastritis. Furthermore, plasmatic ghrelin levels seem to be also a bio-marker of corpus atrophy. Anti-Hp IgG and CagA antibodies as well as PGII levels are able to detect gastric inflammation. Serological parameters could select subjects at risk for gastric mucosa alterations such as inflammation or atrophy, rather than gastric cancer itself. This review analyses the information derived from serological bio-markers as well as the involved clinical studies.
 ...
PMID:Non-invasive tests in gastric diseases. 1843 84

Helicobacter pylori is associated with peptic ulcer and gastric adenocarcinoma. Toll-like receptors (TLRs) participate in H. pylori recognition, and single-nucleotide polymorphisms (SNPs) in TLRs are associated with impaired immune response. We aimed to evaluate the association of TLR2/R753Q and TLR4/D299G/T399I SNPs with gastroduodenal diseases; and study the effect of SNPs on cytokine and chemokine expression in the gastric mucosa. Study included 450 Mexican patients with gastroduodenal diseases. SNPs in TLRs 2 and 4 genes were analyzed by allele-specific PCR. Cytokines and chemokines were assessed by qRT-PCR and immunoassay. TLR4/D299G/T399I polymorphisms were more frequent in duodenal ulcer and showed a trend in gastric cancer, when compared with non-atrophic gastritis. Patients with TLR4 polymorphisms expressed significantly lower levels of IL-1beta, IL-6, IL-8 and GRO-alpha; and higher levels of TNF-alpha, IL-10, MCP-1 and MIP-1alpha . SNPs in TLR4 gene had an association with severe H. pylori-associated disease and with modified pattern of inflammatory cytokines and chemokines in the gastric mucosa. These results suggest that TLR4 SNPs contributes importantly to the clinical outcome of H. pylori infection.
 ...
PMID:TLR4 single-nucleotide polymorphisms alter mucosal cytokine and chemokine patterns in Mexican patients with Helicobacter pylori-associated gastroduodenal diseases. 1875 34

There are few data on circulatory pro-inflammatory cytokine levels and cytokine gene polymorphisms in H. pylori-positive patients. A cross-sectional study was conducted to examine the effects of H. pylori infection, gastric atrophy, and the IL-8 T-251A polymorphism on plasma IL-8 levels in 98 Japanese adults. Seventy-one subjects were positive for H. pylori infection. The geometric mean of plasma IL-8 concentration was significantly higher in subjects with H. pylori infection than in those without (P=0.001). The development of atrophy was negatively associated with IL-8 levels in the H. pylori-positive subjects, although not significantly. Plasma IL-8 levels in the T/T genotype were associated with H. pylori infection and atrophy status (P=0.016). Our findings suggested that circulating IL-8 levels were associated with H. pylori infection. The effect of H. pylori infection on plasma IL-8 levels was not clearly modified by the IL-8 T-251A polymorphism.
 ...
PMID:Associations of plasma IL-8 levels with Helicobacter pylori seropositivity, gastric atrophy, and IL-8 T-251A genotypes. 1971 1

Helicobacter pylori (H. pylori) is an important risk factor of gastric adenocarcinoma. Interleukin (IL)-8 is a potent angiogenic factor and plays an important role in inflammation of gastric mucosa by H. pylori. Host susceptibility may help to predict H. pylori-infected individuals with a higher risk of gastric adenocarcinoma. The aim of this study was to clarify the effect of IL-8 polymorphism on angiogenesis in the process of gastric carcinogenesis in H. pylori-infected Koreans. The IL-8-251A/T polymorphism was genotyped by PCR-RFLP from a total of 395 subjects; 92 normal controls, 87 H. pylori-infected controls, 108 chronic atrophic gastritis and/or intestinal metaplasia and 108 adenocarcinoma. The gastric mucosal concentrations of IL-8, membrane metalloproteinase (MMP)-9, angiopoietin (Ang)-1, and vascular endothelial growth factor (VEGF) were measured by ELISA. MMP-9 concentrations were increased with disease progression. There was significant correlation between MMP-9 and disease progression in AA (r=0.42, p<0.01) and AT genotype (r=0.43, p<0.01). Ang-1 concentrations were increased in AA genotype (r=0.40, p=0.01). However, there was no significant correlation between VEGF and disease progression in AA genotype. In conclusion, IL-8-251 AA genotype may be associated with angiogenesis in gastric carcinogenesis in H. pylori-infected Koreans.
 ...
PMID:The interleukin-8-251 AA genotype is associated with angiogenesis in gastric carcinogenesis in Helicobacter pylori-infected Koreans. 2062 18


1 2 Next >>