| Helicobacter pylori (Hp) infection was now recognized as the primary cause of active chronic gastritis. The organism also appeared to play a pivotal role in peptic ulcer disease, and epidemiological data had also suggested that persistent infection with this bacterium is a risk factor for the development of gastric carcinoma and mucosa-associated lymphoid tissue (MALT) lymphoma in adults. It was also associated with gastro-intestinal diseases such as gastritis, peptic ulcer in children. Hp adhered to gastric epithelium without invading the epithelium. A key question was how these noninvasive bacteria residing in the mucus layer overlying the epithelium produced inflammation and caused damage to the underlying tissue? The present study showed gastric infection with Hp induces the mucosal production of various cytokines in the host, including interleukin-lp(IL-lp), IL-6, IL-8, and tumor necrosis factor a(TNF-a). The goals of this study were to determine the changes of IL-8 and IL-8mRNA in gastric and duodenal mucosa of children with Hp infection and to study the effect of Helicobacter pylori infection on the expression of IL-8 and IL-8 mRNA, and to evaluate its possible roles in the pathogenesis of gastric and duodenal mucosa inflammation of Hp related gastroduodenal diseases.Thirty-six patients who had abdominalgia, nausea, vomiting, abdominal distention, belch and anepithymia (16 boy and 20 girl; age range 5 -114 years, mean 9±2.69 years) referred for endoscope were recruited into this study. None of them had received non-steroidal anti-inflammatory drugs, proton pump inhibitors, antibiotics within previous one month, and they had no previous sever gastro-intestinal diseases. Patients had been advised to stop any antacid drug treatment at least 4 weeks before endoscope. Seven biopsy specimens were taken , using the same size of forceps, from similar topographical sites from the antral and duodenal mucosa on endoscope in patients with or without Hp infection. Four gastric mucosa: one for histological examination, one for urease test and two for IL-8 measurement; three duodenal mucosa: one for histological examination and two for IL-8 measurement. The expression of IL-8 in gastric and duodenal mucosa was measured by ELISA and the result expressed as pg/mg biopsy; the expression of IL-8 mRNA was determined by using RT-PCR.Statistical analysis: all data were changed logarithm, and compared using analysis of variance followed by T test. P<0.05 was considered statistically significant.Inflammation of gastric antral mucosa was more sever in Hp-positive group than that in Hp-negative group. A active inflammation often existed on the basis of chronic inflammation in Hp-positive mucosa, and duodenal mucosa had mild chronic inflammation in Hp-positive group. Of seventeen children who were not infected with Hp, four children had pathologically normal gastric mucosa and twelve children had mild chronic gastritis, only one child had an active chronic gastritis. Ninteen children were infected with Hp and all had chronic gastritis with signs of active inflammation. Gastric and duodenal mucosal IL-8 and IL-8 mRNA were higher in Hp infected than in non infected children (IL-8 in gastric mucosa: 24. 66 - 177. 77pg/mg,2. 94 - 12. 98pg/mg, t=57. 19, p<0. 01; in duodenal mucosa: 4. 28-47. 76pg/mg, 2. 04 - 9. 52pg/mg, t=32. 53, p<0. 01. IL-8 mRNA in gastric mucosa: 2. 37 - 4. 99, 0.05- 0.44, t=500. 84, p<0. 01; in duodenal mucosa: 1.22- 1.87, 0.01- 0.23, t=1084.32, p<0.01). Children with active chronic gastritis had higher interleukin-8 levels and IL-8 mRNA expression than those with inactive gastritis (IL-8 in gastric mucosa: 12.98 - 177. 77pg/mg, 2.04 - 10. 43pg/mg, t=48.04, p<0. 01; in duodenal mucosa: 5.28 - 47. 76pg/mg, 3.19 - 8. 14pg/mg, t=28.31, p<0.01. IL-8 mRNA in gastric mucosa: 0.51 - 4.99,0.01 - 0.44, t=154. 14, p<0. 01; in duodenal mucosa: 0.23 - 1.87,0.01 - 0. 20, t=229. 48, p<0. 01).In conclusion, higher level of IL-8 and expression of IL-8 mRNA were seen in Hp-positive gastric mucosa a... |
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