Impact of Helicobacter pylori infection on gastric and plasma ghrelin dynamics in humans
Impact of Helicobacter pylori infection on gastric and plasma ghrelin dynamics in humans
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DOI：
10.1111/j.1572-0241.2005.41492.x
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发表时间：
2005-08-01
影响因子：
9.8
通讯作者：
Kohno, S
中科院分区：
文献类型：
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作者：
Isomoto, H;Ueno, H;Kohno, S
结论：关于幽门螺杆菌和循环胃饥饿素之间的关系有相互矛盾的报道。我们试图澄清H的影响。pylori感染对胃和血浆ghrelin动力学的影响。采用实时荧光定量聚合酶链反应（PCR）和放射免疫分析法分别检测幽门螺杆菌感染者和25例非幽门螺杆菌感染者胃内ghrelin mRNA表达水平和胃内ghrelin肽含量。我们还测量了血浆ghrelin浓度，并分析了胃底腺区ghrelin免疫反应细胞的数量。51例H. pylori感染者用兰索拉唑、克拉霉素和阿莫西林三联疗法治疗7天。pylori阳性患者（1.64 ± 1.27任意单位）显著低于H.幽门阴性受试者（4.87 +/- 4.1，p < 0.0001）。生长素释放肽含量也有类似的趋势（分别为31.2 +/-27.5和81.2 +/-64.1 ng/mg蛋白，p < 0.0001）。生长素释放肽免疫反应阳性细胞数/mm（2）在H.无菌状态。血浆ghrelin浓度在H.幽门感染的患者（144.6 ± 7.8.8fmol/ml）显著低于未感染的受试者（196.1 ± 97.2，p < 0.05），并且在感染治愈后增加。血浆ghrelin水平与ghrelin mRNA（r = 0.583，p < 0.0001）和肽产物（r = 0.574，p < 0.0001）的表达水平呈正相关。随着腺体萎缩程度的加重，胃Ghrelin mRNA表达（p < 0.05）、肽含量（p < 0.01）和Ghrelin免疫反应阳性细胞密度（p < 0.05）呈明显的递减趋势。慢性炎症的组织学严重程度也对ghrelin mRNA的表达（p < 0.001）和肽的产生（p < 0.005）产生负性影响。幽门螺杆菌感染对胃和血浆生长素释放肽动力学具有负面影响。与感染相关的慢性炎症和萎缩性变化可能影响胃饥饿素的生物合成，并导致低循环水平。
OBJECTIVES: There are contradictory reports on the relationship between Helicobacter pylori and circulating ghrelin. We sought to clarify the influence of H. pylori infection on gastric and plasma ghrelin dynamics in humans.METHODS: Using endoscopic biopsies from the corpus of 56 H. pylori-infected patients and 25 uninfected subjects, ghrelin mRNA expression levels and gastric ghrelin peptide contents were measured by real-time polymerase chain reaction and radioimmunoassay, respectively. We also measured plasma ghrelin concentrations and analyzed the numbers of ghrelin immunoreactive cells in the fundic gland area. Fifty-one patients with H. pylori infection were treated with a 7-day triple therapy consisting of lansoprazole, clarithromycin, and amoxicillin.RESULTS: The gastric ghrelin mRNA expression level of H. pylori-positive patients (1.64 +/- 1.27 in arbitrary units) was significantly lower than in H. pylori-negative subjects (4.87 +/- 4.1, p < 0.0001). A similar trend was noted for ghrelin peptide contents (31.2 +/- 27.5 vs 81.2 +/- 64.1 ng/mg protein, respectively, p < 0.0001). There was no significant difference in the number of ghrelin immunoreactive cells/mm(2) in terms of H. plyori status. Plasma ghrelin concentrations in H. pylori-infected patients (144.6 +/- 7.8.8 fmol/ml) were significantly lower than in uninfected subjects (196.1 +/- 97.2, p < 0.05) and increased following cure of the infection. Plasma ghrelin levels correlated positively with the expression levels of ghrelin mRNA (r = 0.583, p < 0.0001) and peptide products (r = 0.574, p < 0.0001). There was a significant stepwise decrease in gastric ghrelin mRNA expression (p < 0.05), peptide contents (p < 0.01) and density of ghrelin immunoreactive cells (p < 0.05) with progression of histological severity of glandular atrophy in the corpus. The histological severity of chronic inflammation also negatively influenced the ghrelin mRNA expression (p < 0.001) and peptide production (p < 0.005).CONCLUSIONS: H. pylori infection has a negative impact on gastric and plasma ghrelin dynamics. Chronic inflammatory and atrophic changes associated with the infection may affect gastric ghrelin biosynthesis and contribute to the low circulating levels.