CAMPYLOBACTER PYLORIDIS IN GASTRODUODENAL DISEASE

C.胃中的幽门炎与 有消化性溃疡病、非溃疡性消化不良和胃炎。 通过细菌培养或组织学检测微生物 检查需要侵入性的内窥镜检查， 排除了大规模的研究。 我们已经开发并验证了一种可靠的无创呼吸 本试验是基于C.幽门 该测试使用13 C-尿素并检测C的存在。幽门 胃中出现13 CO2引起的感染 呼吸 该测试还测量体内抗生素敏感性 梭幽门螺杆菌及其对药物治疗的反应。 我们建议 研究流行病学，病理学，分子生物学， 免疫学、微生物学等方面的研究。幽门 呼吸测试 将促进快速经济的血清流行病学研究， C.幽门感染 这些研究包括：1）患病率 梭无症状个体中的幽门螺杆菌感染; 2） C.流行胃溃疡、十二指肠溃疡和胃溃疡的患者 溃疡、非溃疡性消化不良和儿童慢性复发 腹痛; 3）C.家族性幽门梗阻 4）解剖学范围和 C的严重性。幽门螺杆菌感染在胃胃炎; 5） C.慢性萎缩性胃炎 胃炎; 6）C.幽门水平， 十二指肠溃疡病复发和7）发展 永久根除C.幽门 最后，我们将评估根除C的后果。 幽门梗阻对胃组织学的影响，对十二指肠溃疡复发的影响， 在非溃疡性消化不良中获得症状缓解。 的 临床研究将提供解决基本问题的机会， 问题：是否存在C。幽门螺杆菌菌株，血清型， 质粒，或DNA杂交组与特定 疾病过程？ 我们还将比较同种型的性质 和对C.幽门感染 一个 将开发ELISA测定法来鉴定那些免疫显性的 C.当前或过去的幽门螺杆菌抗原 感染C.幽门 最后，我们将描述 毒力因子和毒力机制。幽门螺杆菌发病机制

The presence of C. pyloridis in the stomach has been associated with peptic ulcer disease, non-ulcer dyspepsia and gastritis. Detection of the organism by either bacterial culture or histologic examination has required invasive endoscopic procedures which have precluded large scale studies. We have developed and validated a reliable noninvasive breath test based on the high endogenous urease content of C. pyloridis. This test uses 13C-urea and detects the presence of C. pyloridis infection in the stomach by the appearance of 13CO2 in the breath. The test also measures the in vivo antibiotic sensitivity of C. pyloridis and its response to drug treatment. We propose to study the epidemiology, pathology, molecular biology, immunology, and microbiology of C. pyloridis. The breath test will facilitate rapid economical studies of the seroepidemiology of C. pyloridis infections. These studies include: 1) the prevalence of C. pyloridis infection in asymptomatic individuals; 2) the prevalence of C. pyloridis in patients with gastric ulcers, duodenal ulcers, non-ulcer dyspepsia and children with chronic recurrent abdominal pain; 3) the transmission of C. pyloridis among family members; 4) the relationship of the anatomical extent and severity of C. pyloridis infection in the stomach to gastritis; 5) the relationship of C. pyloridis to development of chronic atrophic gastritis; 6) the relationship between C. pyloridis levels and relapse of duodenal ulcer disease and 7) the development of therapeutic regimens that permanently eradicate C. pyloridis. Finally, we will evaluate the consequences of eradicating C. pyloridis on gastric histology,, on relapse of duodenal ulcers and on obtaining symptomatic relief in non-ulcer dyspepsia. The clinical studies will provide the opportunity to address the basic questions: are there individual C. pyloridis strains, serotypes, plasmids, or DNA hybridization groups associated with specific disease processes? We will also compare the nature of the isotype and idiotype antibody response to C. pyloridis infection. An ELISA assay will be developed to identify those immunodominant epitopes of C. pyloridis antigens arising from current or past infection by C. pyloridis. Finally, we will characterize the virulence factors and mechanisms of C. pyloridis pathogenesis.