Interaction Of Pathogenic Bacteria With Leukocytes

致病菌与白细胞的相互作用

• 批准号: 6546348
• 负责人: FRANK R DELEO
• 金额: --
• 依托单位: NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES
• 依托单位国家: 美国
• 资助国家: 美国
• 起止时间: 至
• 项目状态: 未结题
• 来源: https://reporter.nih.gov/project-details/6546348
• 关键词: CD antigens; Staphylococcus aureus; Streptococcus pyogenes; antigen receptors; apoptosis; bacterial proteins; bactericidal immunity; gene induction /repression; host organism interaction; human tissue; immunogenetics; microarray technology; neutrophil; oligonucleotides; phagocytosis; proteomics

Project Goals and Objectives: Specific projects will 1) identify and characterize specific mechanisms used by pathogenic bacteria to evade or subvert normal phagocyte responses and therefore cause disease, and 2) investigate human phagocyte response mechanisms to pathogenic bacteria. Research Accomplishments: 1) We have determined that Group A Streptococcus secretes a homologue of human CD11b that blocks innate and acquired immune function. This represents a novel mechanism by which Group A Streptococcus can survive during the course of human infection. 2)We used human oligonucleotide microarrays (Affymetrix GeneChip) to determine global gene expression profiles in human PMNs during receptor-mediated phagocytosis. We discovered that gene transcription following phagocytosis serves mainly to determine PMN fate. We identified entire apoptotic pathways (>100 genes) for activated human PMNs and for those undergoing spontaneous apoptosis. These studies will be used as a springboard for studies with human pathogens.

项目目标和目标：特定的项目将1）识别并表征病原细菌用来逃避或颠覆正常吞噬细胞反应的特定机制，因此引起疾病，2）研究人类吞噬细胞对致病细菌的反应机制。研究成就：1）我们已经确定A组链球菌分泌了人类CD11b的同源物，该同源物阻断了先天和获得的免疫功能。这代表了一种新的机制，通过该机制，A组链球菌可以在人类感染过程中生存。 2）我们使用人类寡核苷酸微阵列（Affymetrix Genechip）来确定受体介导的吞噬作用期间人PMN中的全球基因表达谱。我们发现吞噬作用后的基因转录主要用于确定PMN命运。我们确定了激活人PMN的整个凋亡途径（> 100个基因）和那些正在自发凋亡的人。这些研究将用作研究人类病原体研究的跳板。