REGULATION OF MACROPHAGE FUNCTION BY COMPONENTS OF WOODSMOKE

木烟成分对巨噬细胞功能的调节

• 批准号: 8167597
• 负责人: CHRISTOPHER Todd MIGLIACCIO
• 金额: $ 15.23万
• 依托单位: UNIVERSITY OF MONTANA
• 依托单位国家: 美国
• 财政年份: 2010
• 资助国家: 美国
• 起止时间: 2010-06-01 至 2011-05-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8167597
• 关键词: Acute; Air; Aryl Hydrocarbon Receptor; Biological Assay; Biomass; Burn injury; Child; Computer Retrieval of Information on Scientific Projects Database; Dioxins; Event; Family; Flow Cytometry; Funding; Grant; Guidelines; Health; Home environment; Human; Hydrocarbons; Immune system; In Vitro; Institution; Knockout Mice; Link; Lung; Methods; Modeling; Molecular; Molecular Biology; Mouse Strains; Mus; Orphan; Particulate; Pathway interactions; Regulation; Research; Research Personnel; Resources; Smoke; Source; Testing; Transgenic Organisms; United States National Institutes of Health; Wood material; base; cigarette smoking; cooking; macrophage; member; receptor binding; respiratory; transcription factor

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Wood smoke (WS) is regulated according to the EPA guidelines for air quality, which are based on urban particulate studies. Wood smoke particulates are not the same as urban particulates, but the specific health effects of WS are not defined. A variety of studies have found increases in acute respiratory illnesses (ARI) in children in homes where biomass burning (i.e. wood) is the method of cooking. Human observations point to strong links between smoke exposure and respiratory illness, but are lacking in the cellular and molecular events that are involved. By contrast, cigarette smoke (CS) research is extensive. Recent studies have linked CS with activation of the aryl hydrocarbon receptor (AhR) and its subsequent activation of the RelB member of the NF¿B family of transcription factors. AhR is an orphan receptor that binds with dioxin and dioxin-like compounds and can promote alterations in the immune system. Several groups have described multiple types of polyaromatic hydrocarbons (PAH) in WS that are the same or similar to those found in CS. We propose to assess the effects of WS components on macrophage function using a murine pulmonary model. Wood smoke-derived alterations in macrophage function will be defined by flow cytometry, molecular biology, transgenic and null mouse strains, and in vitro functional assays. We propose to test the central hypothesis that macrophage function is differentially regulated by components of wood smoke via the aryl hydrocarbon receptor and NF¿B pathway.

该子项目是利用该技术的众多研究子项目之一 资源由 NIH/NCRR 资助的中心拨款提供。 研究者 (PI) 可能已从 NIH 的另一个来源获得主要资金， 因此可以出现在其他 CRISP 条目中 列出的机构是。 中心，不一定是研究者的机构。 木材烟雾 (WS) 是根据 EPA 空气质量指南进行监管的，该指南基于城市颗粒物研究。木材烟雾颗粒物与城市颗粒物不同，但各种研究并未定义 WS 的具体健康影响。研究发现，在以生物质燃烧（即木材）为烹饪方法的家庭中，儿童急性呼吸道疾病 (ARI) 的发病率有所增加。人类观察表明，烟雾暴露与呼吸道疾病之间存在密切联系，但缺乏导致这种疾病的细胞和分子事件。相比之下，香烟烟雾 (CS) 的研究非常广泛，表明 CS 与芳烃受体 (AhR) 的激活及其随后对 NF 的 RelB 成员的激活有关。 AhR 转录因子 B 家族是一种孤儿受体，可与二恶英和二恶英类化合物结合，并可促进免疫系统的改变。一些研究小组已经描述了与 WS 相同或相似的多种类型的多环芳烃 (PAH)。我们建议使用小鼠肺部模型来评估 WS 成分对巨噬细胞功能的影响，这将通过流式细胞术、分子生物学、转基因和无效小鼠来定义。我们建议测试以下中心假设：巨噬细胞功能通过芳烃受体和 NF 受木烟成分的差异调节。 B途径。