[ 摘要 ]
幽門桿菌是人類胃部主要的病原菌，利用鞭毛的運動性，進入胃黏膜層，並分泌各種細胞毒素，使得胃黏膜受到損傷及發炎，藉著削弱黏膜的防禦，導致慢性胃炎，並且經過萎縮性胃炎、小腸化生及細胞分化異常等病理進程，最後發展為胃癌，目前幽門桿菌已經被確認為致癌因子。胃黏液蛋白在胃部形成保護屏障以及潤滑等功能，是阻擋幽門桿菌感染的第一防線。正常胃部在表面黏液細胞和頸黏液細胞表現MUC1和MUC5AC，而MUC6經由胃竇處的幽門腺以及胃體處的頸黏液細胞分泌，MUC2並沒有在正常胃上皮表現。在胃癌及癌症前趨病灶 (precancerous lesion)，隨著胃癌發展的進程，MUC1、MUC5AC和MUC6的表現量減少，而MUC2則增加表現量。因此黏液蛋白的表現差異，能夠評估胃癌病變 (gastric carcinogenesis)的程度。同時感染幽門桿菌會造成上皮細胞增生，利用細胞核抗原Ki-67的表現評估細胞增生的情況，作為幽門桿菌感染導致早期惡性細胞轉型的生物指標。臺灣東部地區原住民 (aborigine)在遺傳因素、文化背景、生活飲食習慣、衛生健康概念以及生活環境，與非原住民族群 (nonaborigine)有極大之差異。族群間的差異可能影響幽門桿菌感染所造成的疾病嚴重程度，因此本篇研究目的為分析在兩種族群幽門桿菌感染導致胃部疾病的過程中，胃黏蛋白群表現的轉變情形，以瞭解宿主胃部黏蛋白群的改變與疾病徵兆之關係。
實驗結果發現原住民和非原住民族群感染幽門桿菌皆會導致胃黏液的分泌量降低，而感染幽門桿菌的原住民族群胃黏液分泌量又較非原住民族群更低；在四種黏液蛋白表現量方面，黏液蛋白MUC1和MUC6的表現在原住民及非原住民族群的CLOtest陽性或陰性檢體與疾病之間，表現的程度沒有顯著差異，而在CLOtest陽性檢體的原住民和非原住民族群，MUC2的表現量較CLOtest陰性的檢體增加，MUC5AC的表現量則較陰性檢體減少；在感染幽門桿菌的宿主，發現以Ki-67作為評估的細胞增生指數增加，顯示感染幽門桿菌會造成細胞增生，而非原住民族群的細胞增生情況又較原住民高。
由以上實驗結果得知，在不同族群的宿主感染幽門桿菌後，造成胃黏液分泌量、黏液蛋白的表現以及細胞增生等有明顯的差異，因此在不同族群之間，對於胃癌的篩檢或風險的評估，並不能以一概全，而本研究提供為臨床診斷胃部疾病的另一指標。

[ 英文摘要 ]
Helicobacter pylori is the main pathogen of human stomach and has flagellar to colonize the gastric mucosa led to inflammation. H. pylori causes chronic gastritis which progresses to cancer through atrophy, metaplasia, and dysplasia. Mucin proteins construct gastric mucus which is the first line of defense and protects gastric mucosa from H. pylori infection. In the normal stomach, MUC1 and MUC5AC secrete from surface mucus cells and mucous neck cells and MUC6 secret from pyloric glands of antrum and mucous neck cells of corpus. MUC2 do not expression in the normal gastric mucosa. Changes in the immunohistochemical characteristics are linked with the pathogenesis. The mucin proteins expression profiles showed to classify the progressive stages of human gastric epithelial pathogenesis. Furthermore, H. pylori infection causes gastric epithelial cell proliferation and the Ki-67 protein which is a nuclear protein tightly associated with cell proliferation is a known associated factor for gastric cancer. There is much different in heredity, culture, live styles, hygiene, and live environment from aborigine and nonaborigine in eastern Taiwan. The differences of races might affect the outcome of H. pylori infected disease. The aim of this study was to compare the profiles of mucin proteins expression with H. pylori-infected hosts in eastern Taiwan and to clarify the relationship between the changes of mucin proteins expression and H. pylori-infected disease.
The mucus secretion of H. pylori-infected hosts was lower than non-infected ones. Within H. pylori-infected hosts, aborigine had much lower mucus secretion. Compared H. pylori-infected aborigine with non-infected aborigine in the expression of mucin proteins, H. pylori-infected aborigine was increase in MUC2 expression but decrease in MUC5AC expression. Moreover, Ki-67 protein expression index was much more increase in H. pylori-infected non-aborigine than aborigine. Above theses manifestations indicated that there might be different outcome from the pathological diagnosis of the H. pylori-infected non-aborigine and aborigine to express distinct immunohistological markers which may be helpful in prediction the prognosis.