Expression In Gastric Tissues Research Articles

Inflammatory gene profiles in gastric mucosa during Helicobacter pylori infection in humans.

Helicobacter pylori infection is associated with an inflammatory response in the gastric mucosa, ultimately leading to cellular hyperproliferation and malignant transformation. Hitherto, only expression of a single gene, or a limited number of genes, has been investigated in infected patients. cDNA arrays were therefore used to establish the global pattern of gene expression in gastric tissue of healthy subjects and of H. pylori-infected patients. Two main gene expression profiles were identified based on cluster analysis. The data obtained suggest a strong involvement of selected Toll-like receptors, adhesion molecules, chemokines, and ILs in the mucosal response. This pattern is clearly different from that observed using gastric epithelial cell lines infected in vitro with H. pylori. The presence of a "Helicobacter-infection signature," i.e., a set of genes that are up-regulated in biopsies from H. pylori-infected patients, could be derived from this analysis. The genotype of the bacteria (presence of genes encoding cytotoxin-associated Ag, vacuolating cytotoxin, and blood group Ag-binding adhesin) was analyzed by PCR and shown to be associated with differential expression of a subset of genes, but not the general gene expression pattern. The expression data of the array hybridization was confirmed by quantitative real-time PCR assays. Future studies may help identify gene expression patterns predictive of complications of the infection.

Human stomach-specific gene, CA11, is down-regulated in gastric cancer.

To reveal the implication in gastric cancer pathogenesis of the novel human gene referred to as CA11, which was recently isolated by a differential display technique using normal gastric mucosa and gastric cancer tissue, we examined CA11 expression in 50 primary gastric cancers and also introduced the CA11 gene into gastric cancer cells. RNA dot blot analysis against various human organs and developmental stages demonstrated that CA11 was intensively expressed especially in normal stomach tissue. Northern blot analysis showed that expression of the CA11 gene in cancer tissue was down-regulated compared with normal tissue. Semi-quantitative RT-PCR also demonstrated that CA11 gene expression was decreased in 41 out of 50 (82%) of the gastric cancer tissues, when compared with normal stomach tissues, while no relationship was found between CA11 expression and various clinicopathological characteristics including histological type, depth of invasion, lymph node metastasis, and clinical stage. Immunohistochemical analysis with anti CA11 antibody showed that CA11-positive staining was observed in the surface regions of normal gastric epithelium, but was found faintly or not at all in cancer tissues. CA11 transfected MKN28 cells also displayed a marked decrease in the number of colony formations when compared to double normal controls. These findings suggest that the loss of CA11 expression in gastric tissues may play an important role in gastric carcinogenesis.

Proinflammatory cytokine expression in gastric tissue from children with Helicobacter pylori-associated gastritis.

Helicobacter pyloriinfection of the gastric mucosa in humans is usually acquired early in life. The chronic inflammation that ensues involves the increased production of inflammatory cytokines. Published data on production of these mediators by gastric mucosa of H. pylori-infected children are few. Seventy-nine children, aged 5 to 18 years, referred for upper gastrointestinal endoscopy to four separate hospitals in Chile, were studied. The concentrations of interleukin (IL)-1beta, IL-6, IL-8, and tumor necrosis factor alpha were measured in homogenates of gastric mucosal biopsy specimens. Cytokine expression was confirmed by reverse transcription polymerase chain reaction. These data were correlated with the patients' clinical, histologic and sociodemographic status. Patient rate of colonization by H. pylori was inversely correlated with socioeconomic status (P < 0.005) and positively correlated with age (P < 0.0025). In gastric mucosa, concentrations of IL-1beta, IL-8, and tumor necrosis factor alpha were all significantly higher in H. pylori-positive patients than in H. pylori-negative patients and in patients who had histologic gastritis than in those with normal gastric mucosa. In patients with peptic ulcer disease, only IL-1beta and IL-8 concentrations were significantly elevated when compared with those of patients without ulcers. Interleukin-6 concentrations were comparable among the different groups analyzed. This study suggests that increased gastric mucosal production of the proinflammatory cytokines IL-1beta and IL-8 is probably involved in H. pylori-associated gastric damage in children and may be crucial in determining the different clinical outcomes.

Proinflammatory Cytokine Expression in Gastric Tissue From Children With Helicobacter pylori–Associated Gastritis

ABSTRACTBackgroundHelicobacter pylori infection of the gastric mucosa in humans is usually acquired early in life. The chronic inflammation that ensues involves the increased production of inflammatory cytokines. Published data on production of these mediators by gastric mucosa of H. pylori–infected children are few.MethodsSeventy‐nine children, aged 5 to 18 years, referred for upper gastrointestinal endoscopy to four separate hospitals in Chile, were studied. The concentrations of interleukin (IL)‐1β, IL‐6, IL‐8, and tumor necrosis factor α were measured in homogenates of gastric mucosal biopsy specimens. Cytokine expression was confirmed by reverse transcription polymerase chain reaction. These data were correlated with the patients' clinical, histologic and sociodemographic status.ResultsPatient rate of colonization by H. pylori was inversely correlated with socioeconomic status (P &lt; 0.005) and positively correlated with age (P &lt; 0.0025). In gastric mucosa, concentrations of IL‐1β, IL‐8, and tumor necrosis factor α were all significantly higher in H. pylori–positive patients than in H. pylori–negative patients and in patients who had histologic gastritis than in those with normal gastric mucosa. In patients with peptic ulcer disease, only IL‐1β and IL‐8 concentrations were significantly elevated when compared with those of patients without ulcers. Interleukin‐6 concentrations were comparable among the different groups analyzed.ConclusionsThis study suggests that increased gastric mucosal production of the proinflammatory cytokines IL‐1β and IL‐8 is probably involved in H. pylori–associated gastric damage in children and may be crucial in determining the different clinical outcomes.