REGULATION OF ENTERIC HYPEROXALURI BY OXALOBACTER

产状草杆菌，一种新发现的定植细菌 所有脊椎动物的胃肠道(GI)都有 由于其重要的共生关系而受到极大的关注 它的宿主也调节肠道中草酸的吸收 作为血浆中草酸水平的两个因素与风险相关 发展成草酸钙肾结石。草酸是一种副产品 新陈代谢和大多数饮食的共同成分；然而，如果 如果允许积聚，它可能会导致许多病理情况， 包括高草酸尿、心脏电导障碍、草酸钙 结石，肾功能衰竭，死亡，可能还有炎症性肠病 外阴前庭炎。尽管甲型假单胞菌的潜在意义 控制肠源性高草酸尿症，从而与草酸相关 精神障碍，研究由于先天的困难而受到限制 培养和鉴定这种细菌。尽管如此，初步的 研究已经表明，蜂群的数量与 草酸杆菌的形成单位。每克粪便的数量和频率 复发性尿路结石、炎症性肠病和 囊性纤维化中的高草酸尿/肾钙沉着症。随着时代的发展 一种快速而灵敏的基于DNA的检测系统 ，我们现在能够研究它们之间的相关性 尿石症的风险增加和福尔马氏杆菌的缺失 胃肠道。以实验大鼠为模型，我们提出：1) 不同亚系非定植大鼠的定植研究 以确定甲氧西林的疗效是否存在变异 不同的产甲氧西林杆菌菌株的定植，如果是原发的 定植排除了二次定殖，2)决定了O。 甲状旁腺素可以预防高草酸尿和随后形成的 不同亚型草酸钙结晶在大鼠体内的定植 细菌和高草酸饮食的挑战，以及3) 检查饮食和/或抗生素治疗之间的关系 已知的O.formgeres随后对GI区的非殖民化 在人类人口中发生的情况以及GI地区的非殖民化 是不可逆转的。这些研究的结果应该为我们提供关于 产甲假单胞菌在调节植物体内草酸平衡中的作用 脊椎动物，包括人类，应该在 草酸相关疾病的预防治疗，如复发 肾结石形成。

Oxalobacter formigenes, a recently identified bacterium that colonizes the gastrointestinal (GI) tracts of all vertebrates, has gained considerable attention due to its important symbiotic relationship with its hosts in regulating oxalic acid absorption in the intestines as well as oxalic acid levels in plasma two factors associated with the risk to develop calcium-oxalate kidney stones. Oxalic acid is a by-product of metabolism and a common constituent of most diets; however, if permitted to accumulate, it can cause numerous pathological conditions, including hyperoxaluria, cardiac conductance disorders, calcium oxalate stones, renal failure, death and possibly inflammatory bowel disease and vulvovestibulitis. Despite the potential significance of O. formigenes in controlling enteric hyperoxaluria, and thus oxalate-related disorders, research has been limited due to inherent difficulties in culturing and identifying this bacterium. Nevertheless, preliminary studies already suggest a correlation between the number of colony forming units of Oxalobacter sp. per gram feces and the frequency of recurrent urolithiasis, inflammatory bowel disease and hyperoxaluria/nephrocalcinosis in cystic fibrosis. With the development of a rapid and sensitive DNA-based detection system highly specific for O. formigenes, we are now able to investigate the correlation between an increased risk for urolithiasis and the absence of O. formigenes from the GI tract. Using the laboratory rat as a model, we propose to: 1) study the colonization of non-colonized rats with various sub-strains of O. formigenes to determine if variations exist in the efficacy of different strains of O. formigenes to colonize and if primary colonization precludes secondary colonizations, 2) determine whether O. formigenes can prevent hyperoxaluria and subsequent formation of calcium-oxalate crystals in rats colonized with various sub-strains of the bacterium and challenged with high oxalate-containing diets, and 3) examine the relationship between diet and/or antibiotic treatment with subsequent decolonization of the GI tract by O. formigenes known to occur in human populations and whether decolonization of the GI tract is irreversible. Results from these studies should provide insight into the role O. formigenes plays in regulating oxalate homeostasis in vertebrates, including humans, and should offer new modalities in prevention therapy for oxalate-associated disorders, such as recurrent kidney stone formation.