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Pathways regulating amoebic cyst formation

调节阿米巴包囊形成的途径

基本信息

批准号：
7567609
负责人：
DANIEL J EICHINGER
金额：
$ 39.3万
依托单位：
NEW YORK UNIVERSITY SCHOOL OF MEDICINE
依托单位国家：
美国
项目类别：
财政年份：
2000
资助国家：
美国
起止时间：
2000-03-01 至 2011-01-31
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/7567609
关键词：
Abbreviations Acids Affect Cells Cessation of life Colon Culture Media Cyst Developmental Process Differentiation Antigens Disease Entamoeba Entamoeba histolytica Eukaryota Family Galactose Gene Expression Gene Proteins Glucose Goals Growth Histone Deacetylase Histones Intestines Lectin Life Cycle Stages Ligand Binding Location Maintenance Messenger RNA Modification Molecular Mucous body substance Nucleosomes Open Reading Frames Organ Orthophosphate Dikinase Pyruvate Parasites Pathway interactions Ploidies Poly(A)-Binding Proteins Population Process Production Proteins Reaction Sodium Butyrate Staging Stimulus Surface Trichostatin A Triton X100 Urea Volatile Fatty Acids Work deprivation design experience histone acetyltransferase histone modification mRNA Differential Displays member protein expression research study response

项目摘要

DESCRIPTION (provided by the applicant): Entamoeba histolytica infects approximately 1% of the world's population, and causes up to 100,000 deaths annually. The disease-causing trophozoite stage of the parasite differentiates into the infectious cyst form while within the host colon, and the stimuli that induce this differentiation are only now becoming clear. We had previously found that galactose-terminated molecules, including those in colonic mucus, are used by the trophozoites to form cellular aggregates just prior to cyst formation. We have now found that short chain fatty acids, which are produced by the resident colonic bacterial population, can regulate the Entamoeba cyst formation process in a concentration-dependent manner. The effects of short chain fatty acids on the parasites are different from the effects these compounds have on other cells of the host, but they may be working through similar molecular mechanisms. This project will examine the mechanism(s) whereby these compounds regulate cyst formation, and will determine the extent of the effects these compounds have on gene and protein expression in the parasite.

描述(由申请人提供)：溶解组织内阿米巴感染了大约1%的世界人口，每年导致多达10万人死亡。寄生虫致病的滋养体阶段在宿主结肠内分化为感染性包囊形式，而诱导这种分化的刺激因素直到现在才变得清晰。我们之前已经发现，半乳糖终止的分子，包括那些在结肠粘液中的分子，在包囊形成之前被滋养体用来形成细胞聚集体。我们现在发现，由常驻结肠细菌群产生的短链脂肪酸可以浓度依赖的方式调节内阿米巴包囊的形成过程。短链脂肪酸对寄生虫的影响与这些化合物对宿主其他细胞的影响不同，但它们可能通过类似的分子机制发挥作用。该项目将研究这些化合物调节包囊形成的机制(S)，并将确定这些化合物对寄生虫基因和蛋白质表达的影响程度。