PATHOGENESIS OF ALLERGIC DISEASES OF THE SKIN & LUNGS

纽约州立大学石溪分校过敏性疾病中心研究致病因素 组织损伤机制在多种疾病中的作用 包括身体原因引起的麻疹、慢性荨麻疹和血管性水肿， 遗传性血管性水肿、莱姆病、冷球蛋白血症(及其他 脉管炎)和哮喘。我们将研究其分子机制。 嗜碱性粒细胞和肥大细胞释放组胺，激活 经典的补体途径，以及凝血的激活- 激肽途径，如应用于这些疾病。我们将开发新的 人类疾病聚焦中激肽形成的评估方法 激肽原的裂解及缓激肽及其相关物质的测定 降解产物。我们将对组胺进行提纯和表征 释放因子(S)(Hrf)是从 淋巴细胞和/或单核细胞导致嗜碱性粒细胞和肥大细胞 脱颗粒及其与组胺释放的关系 我们已经确定的细胞因子，如白介素3和GM-CSF。我们 将研究温度变化的可能机制 促组胺释放在寒冷性荨麻疹中的作用 低温蛋白质引起的温度(热幅) 冷球蛋白血症的冷沉淀和补体激活。 神经肽作为麻疹的媒介的作用将被评估， 尤其是胆碱能性荨麻疹，我们会 继续研究调解人释放的时间进程和 慢性特发性荨麻疹的组织学评价及临床意义 血管性浮肿。非坏死性血管周围炎症 慢性荨麻疹将被比作血管炎 冷球蛋白血症、晚期反应和接触性皮炎。 我们对遗传性血管性水肿的评估将包括新的方法。 对于各种类型的诊断，氯NIH合成的评估 在体外，并鉴定血管活性物质 导致肿胀。莱姆病是长岛的地方病， 蔓延到整个东北地区。我们计划开发新的、 更准确、更具体的诊断方法，研究免疫 对B.burgdorfei的反应性，并评估其激活能力 感染和Herxheimer反应过程中的介质系统 与治疗有关。最后，我们将研究 可吸入颗粒物分布与哮喘的相关性研究 与形成限流等力学参数的关系 节段、阻塞性呼吸参数和粘液纤毛 通行证。

The Allergic Diseases Center at SUNY-Stony Brook studies pathogenic mechanisms of tissue injury in a wide variety of diseases to include physically induced hives, chronic urticaria and angioedema, hereditary angioedema, Lyme disease, cryoglobulinemia (and other vasculitides) and asthma. We will study molecular mechanisms of histamine release from basophils and mast cells, activation of the classical complement pathway, and activation of the coagulation- kinin pathway, as applied to these diseases. We will develop new methods for assessment of kinin formation in human disease focusing upon cleavage of kininogen and determination of bradykinin and its degradation products. We will purify and characterize Histamine Releasing Factors(s) (HRF) which are cytokines released from lymphocytes and/or monocytes to cause basophils and mast cell degranulation and determine its relationship to histamine-releasing cytokines we have identified such as interleukin 3 and GM-CSF. We will study possible mechanisms by which a temperature change initiates histamine release in cold urticaria and the role of temperature (thermal amplitude) of cryoproteins to cause cryoprecipitation and complement activation in cryoglobulinemia. The role of neuropeptides as mediators of hives will be assessed, particularly as they pertain to cholinergic urticaria, and we will continue studies of the time course of mediator release and histologic assessment of chronic idiopathic urticaria and angioedema. The non-necrotizing perivascular inflammation of chronic urticaria will be compared to the vasculitis of cryoglobulinemia, late phase reactions, and contact dermatitis. Our assessment of hereditary angioedema will include new methods for diagnosis of the various types, assessment of Cl NIH synthesis in vitro, and identification of the vasoactive substance which causes the swelling. Lyme disease is endemic on Long Island and spreading throughout the Northeast. We propose to develop new, more accurate and specific methods of diagnosis, study immune responsiveness to B. burgdorfei, and assess its ability to activate mediator systems during infection and during Herxheimer reactions associated with therapy. Finally, we will study the interrelationship of distribution of inhaled particles in asthma with mechanical parameters such as the formation of flow-limiting segments, obstructive ventilatory parameters, and mucociliary clearance.