Cell Signaling of Host Defense

国立环境卫生科学研究所呼吸生物学实验室校内研究部宿主防御小组，由Michael B领导。Fessler，MD现在进入了自成立以来在NIEHS的第四个年头。我们已经发布了几份报告： 1. 定义了核受体肝X受体在调节肺先天免疫中的新作用的原始出版物（SmoakK等，免疫学杂志2008;180（5）：3305-12） 2. 一项使用蛋白质组学的研究已经鉴定了巨噬细胞对脂多糖（一种环境先天免疫刺激物）的应答中的新事件（Dhungana S等，Mol Cell Proteomics 2009; 8：201-13） 3. 一份报告使用国家调查数据确定了美国人群中血清胆固醇和哮喘之间的新关联（Fessler MB等人，J Allergy Clin Immunol 2009，出版中）。 4. 2篇关于蛋白质组学方法的综述文章（Dhungana S等人，方法Mol Biol 2009 a和2009 b） 5. 关于Toll样受体在代谢综合征中的作用的综述文章（FesslerMB等，Curr Opin Lipidol 2009） 6. 关于中性粒细胞向肺募集的机制的综述文章（Cai等人，Am J Respir Cell Mol Biol 2009，出版中）。 此外，另外一篇描述硬脂酰辅酶A去饱和酶在动脉粥样硬化中的新作用的合作论文正在为动脉粥样硬化、动脉粥样硬化和血管生物学进行修订，另外4篇手稿最近已提交给细胞代谢杂志（描述了载脂蛋白AI在先天免疫中的新作用），血液（描述血脂异常对肺宿主防御的影响），过敏（描述了美国人群中血清胆固醇和特应性之间的新流行病学关联），和过敏和临床免疫学杂志（描述了尘螨过敏原的结构，我们的小组和NIEHS结构生物学实验室合作）。 自我们上次报告以来的其他成就包括博士后研究员小组成员大卫德雷珀博士获得2010年优秀研究员奖。和Jim Aloor博士收到一个抽象的旅行奖，并邀请在2009年美国胸科学会国际会议上向大卫德雷珀院士做口头报告，由小组成员凯瑟琳·斯莫克（Kathleen Smoak）发表（生物学家）在2009年病原体受体的基石会议上的口头报告（加拿大班夫），Fessler博士举办了5次区域研究研讨会，并由Fessler博士主持科学研讨会，并在2009年美国胸科学会国际会议上主持海报会议。 此外，在实验室的5个活跃的研究项目中收集了大量数据：1）载脂蛋白A-I和载脂蛋白E作为肺宿主防御调节剂的特征; 2）胆固醇转运蛋白ABCG 1在肺宿主防御中的作用的特征; 3）用脂肪酸棕榈酸酯修饰的巨噬细胞蛋白的蛋白质组学鉴定。

The Host Defense Group of the Laboratory of Respiratory Biology, Division of Intramural Research, National Institute of Environmental Health Sciences, headed by Michael B. Fessler, MD now enters its fourth year at the NIEHS since inception. We have now published several reports: 1. an original publication that defines a novel role for the nuclear receptor Liver X Receptor in modulation of pulmonary innate immunity (Smoak K et al., Journal of Immunology 2008;180(5):3305-12) 2. an investigation using proteomics that has identified novel events in the response of the macrophage to lipopolysaccharide, an environmental innate immune stimulus (Dhungana S et al., Mol Cell Proteomics 2009; 8:201-13) 3. a report identifying a novel association between serum cholesterol and asthma in the U.S. population, using national survey data (Fessler MB et al., J Allergy Clin Immunol 2009, in press). 4. 2 review articles on proteomic methodology (Dhungana S et al., Methods Mol Biol 2009a and 2009b) 5. a review article on the role of Toll like Receptors in metabolic syndrome (Fessler MB et al., Curr Opin Lipidol 2009) 6. a review article on mechanisms of neutrophil recruitment to the lung (Cai et al., Am J Respir Cell Mol Biol 2009, in press). In addition, one additional collaborative paper that describes a novel role for stearoyl-CoA desaturase in atherosclerosis is under revision for Arteriosclerosis, Thombosis, and Vascular Biology, and 4 additional manuscripts have recently been submitted to the journals Cell Metabolism (describes a novel role for apolipoprotein AI in innate immunity), Blood (describes effect of dyslipidemia on pulmonary host defense), Allergy (describes a new epidemiologic association between serum cholesterol and atopy in the U.S. population), and Journal of Allergy and Clinical Immunology (describes the structure of a dust mite allergen in a collaboration between our Group and the NIEHS Laboratory of Structural Biology). Additional accomplishments since our last report include receipt of a 2010 Fellow Award for Research Excellence by postdoctoral fellow Group members David Draper, Ph.D. and Jim Aloor, Ph.D., receipt of an abstract travel award as well as invitation to deliver an oral presentation to fellow David Draper at the 2009 American Thoracic Society International Conference, delivery by Group member Kathleen Smoak (biologist) of an oral presentation at the 2009 Keystone Conference on Pathogen Receptors (Banff, Canada), delivery of 5 regional research seminars by Dr. Fessler, and Chairing by Dr. Fessler of a Scientific Symposium as well as Facilitation of a poster session at the 2009 American Thoracic Society International Conference. In addition, substantial data has been collected on 5 active research projects in the laboratory: 1) characterization of apoplipoprotein A-I and apolipoprotein E as regulators of pulmonary host defense; 2) characterization of the role of the cholesterol transporter ABCG1 in pulmonary host defense; and 3) proteomic identification of macrophage proteins that are modified with the fatty acid palmitate.