INTERACTIONS OF E HISTOLYTICA WITH HOST MUCOSAL DEFENSES

溶组织内阿米巴是寄生虫致死的第三大原因 疾病，然而，决定一种菌株引起 人们对侵袭性阿米巴病知之甚少。研究的重点是 与肠粘膜相互作用的差异 潜在入侵性组织裂殖吸虫和共生原生动物E. DISPAR，应提供对 肠子。才能成功入侵。溶组织棘球绦虫滋养体必须 绕过许多针对SIgA的免疫和非免疫宿主防御 活化的中性粒细胞及其氧化的杀菌活性 产品。我们将评估组织裂解杆菌和裂解乳杆菌之间的相互作用。 通过以下方式消除宿主粘膜防御： 目的1.评价SIgA在预防阿米巴感染中的作用 免疫SIgA对滋养体结合的影响及其对免疫功能的影响 诱导炎性细胞因子反应，裂解SIgA。 溶组型半胱氨酸蛋白酶的表达及特异性SIgA对其影响 侵袭人体肠道异种移植物。 目的2.比较溶组织乳杆菌和致病乳杆菌对细菌的敏感性。 检测中性粒细胞及其氧化能力的氧化攻击 杀灭溶组织性肠杆菌和散发性肠杆菌的产品，比较抗氧化剂 溶组织肠杆菌、迪帕尔肠杆菌和兰氏革兰氏菌的活性测定 SIgA或Ig G阻断抗氧化活性的能力，并评价 抗氧化剂基因的调控。 目的3.评价阻断抗氧化剂对阿米巴的影响 29kD抗氧化剂和超氧化物的消融表达侵袭 利用反义RNA表达溶组埃希氏菌中的超氧化物歧化酶 溶组织乳杆菌的抗氧化性基因，并检测其重要性。 抗氧化剂对人异种肠道移植瘤侵袭的影响。 通过提供关于寄生虫和宿主因素的重要新见解， 确定感染溶组织性肠杆菌和E。 迪帕尔，这些研究将增加我们对基本宿主的了解 肠道防御系统。

Entamoeba histolytica is the third leading cause of death from parasitic disease, yet the factors which determine the ability of a strain to cause invasive amebiasis are poorly understood. Studies focused on the differences between the interactions with the intestinal mucosal of potentially invasive E. histolytica and the commensal protozoan, E. dispar, should provide important insights into basic host defenses in the bowel. For successful invasion. E. histolytica trophozoites must circumvent a number of immune and non-immune host defenses against sIgA and the microbicidal activity of activated neutrophils and their oxidative products. We will evaluate the interactions of E. histolytica and E. dispar with host mucosal defenses by: Aim 1. Evaluate the role of sIgA in protection against amebic infection by evaluating the effect of immune sIgA on trophozoite binding and on the induction of an inflammatory cytokine response, cleavage of sIgA by the E. histolytica cysteine proteinase, and the effect of specific sIgA on invasion in human intestinal xenografts. Aim 2. Compare the susceptibility of E. histolytica and E. dispar to oxidative attack by testing the ability of neutrophils and their oxidative products to kill E. histolytica and E. dispar, comparing the antioxidant activity of E. histolytica, E. dispar and G. lamblia, determining the ability of sIgA or IgG to block antioxidant activity, and evaluating the regulation of the antioxidant gene. Aim 3. Evaluate the effect of blocking antioxidant activity on amebic invasion by ablating expression of the 29 kD antioxidant and superoxide dismutase in E. histolytica by antisense RNAs, transfecting E. dispar with the antioxidant gene for E. histolytica, and testing the importance of antioxidant activity on invasion of human intestinal xenografts. By providing important new insights into parasite and host factors which determine the outcome of infection invade with E. histolytica and E. dispar, these studies will increase our knowledge of the basic host defenses in the bowel.