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首页> 外文期刊>Journal of Medicine: Clinical, Experimental and Theoretical >Different effects of H. pylori water extracts on cytokines, pepsinogen C and gastrin mucosal release in patients with or without duodenal ulcer.
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Different effects of H. pylori water extracts on cytokines, pepsinogen C and gastrin mucosal release in patients with or without duodenal ulcer.

机译:H.幽门螺杆菌水提取物对细胞因子,胃肠杆菌和胃泌素粘膜粘膜释放或不含十二指肠溃疡的不同效果。

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In the present study we ascertained whether cagA positive and negative H. pylori strains release water soluble products that can influence the production of gastric mucosal cytokines and endocrine (gastrin) or exocrine (pepsinogen C) secretion in 23 H. pylori positive and 19 H. pylori negative patients. Antral biopsies were obtained to classify inflammation, activity, atrophy, intestinal metaplasia and H. pylori density grade. The cagA gene was identified by means of the polymerase chain reaction (PCR) in H. pylori positive colonies after culture of mucosal samples. Three antral biopsies from each patient were incubated with (1.) Water extracts from cagA positive, (2.) Water extracts from cagA negative strains or (3.) H2O (control) at 37 degrees C in a CO2 incubator for 24 hrs. Gastrin, pepsinogen C, IL-1 beta, IL-8, GMCSF, and TNF alpha were measured in the supernatants and mucosal homogenates. H. pylori infection was significantly associated with an increased antral inflammation and activity (chi 2 = 21.7, p < 0.001 and chi 2 = 42.0, p < 0.001), and increased mucosal levels of IL-1 beta, IL-8 and TNF alpha. Water extracts from cagA positive strains enhanced the release of PGC in mucosal biopsy supernatants (p < 0.05) when patients were considered overall and the release of TNF alpha (p < 0.05) when only patients with duodenal ulcer were considered. Water extracts from cagA negative strains stimulated gastrin secretion (p < 0.05). None of the remaining cytokines were influenced by H. pylori water extracts. In conclusion, pepsinogen C and TNF alpha can be induced by cagA positive water extracts and may contribute to damage the gastric and duodenal mucosa. Our findings indicate that in patients with H. pylori infection the increase of the mucosal levels of IL-1 beta and IL-8 does not depend on H. pylori water soluble products, but probably depends on the entire bacterium.
机译:在本研究中,我们确定了CAGA阳性和阴性H.幽门螺杆菌菌株释放水溶性产品,这些产品可影响胃粘膜细胞因子和内分泌(胃泌素)或外分泌(胃肠原C)分泌23小时幽门阳性和19小时。幽门螺杆菌阴性患者。获得肛门活组织检查,以分类炎症,活性,萎缩,肠道成钙和H.幽门螺杆菌密度等级。通过在粘膜样品培养后通过H.幽门螺杆菌阳性菌落中的聚合酶链反应(PCR)鉴定CAGA基因。将来自每位患者的三个嗜烟活组织检查与来自Caga阴性菌株或(3)在37摄氏度的CAG阴性菌株或(3)的水提取物中的水提取物一起温育。在上清液和粘膜匀浆中测量胃泌素,胃蛋白酶C,IL-1β,IL-8,GMCOSF和TNFα。 H.幽门螺杆菌感染与增加的胃窦炎炎症和活性显着相关(CHI 2 = 21.7,P <0.001和CHI 2 = 42.0,P <0.001),以及增加IL-1β,IL-8和TNFα的粘膜水平。 CAGA阳性菌株的水提取物增强了PGC在粘膜活检上清液中的释放(P <0.05)当患者被考虑并释放TNFα(P <0.05)时,只考虑十二指肠溃疡患者。 Caga阴性菌株的水提取物刺激胃泌素分泌(P <0.05)。剩余的细胞因子均未受到幽门螺杆菌水提取物的影响。总之,胃蛋白酶原C和TNFα可以通过CAGA阳性水提取物诱导,可能有助于损害胃和十二指肠粘膜。我们的研究结果表明,在幽门螺杆菌患者中,IL-1β和IL-8的粘膜水平的增加不依赖于幽门螺杆菌水溶性产物,但可能取决于整个细菌。

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