Degenerative changes in the taste system

味觉系统的退行性变化

基本信息

批准号：
8012264
负责人：
LYNNETTE Marie MCCLUSKEY
金额：
$ 26.94万
依托单位：
AUGUSTA UNIVERSITY
依托单位国家：
美国
项目类别：
财政年份：
2003
资助国家：
美国
起止时间：
2003-07-01 至 2014-01-31
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/8012264
关键词：
Accounting Adult Affect Amiloride Animal Feed Anterior Apoptosis Award Bilateral Cell Communication Cell physiology Cells Contralateral Diet Dietary Sodium Epithelial Equilibrium Functional Imaging Gray unit of radiation dose Health Immune Immune response Immune system Injury Interleukin-12 Interleukins Lead Left Leukocytes Maps Mediating Natural regeneration Nerve Neurons Peripheral nerve injury Play Population Proteins Rattus Receptor Cell Recruitment Activity Resolution Right-On Role Sagittaria Sensory Sensory Receptors Side Site Sodium Sodium Channel Stimulus System Taste Buds Taste Perception Testing Tongue Vascular Cell Adhesion Molecule-1 Work afferent nerve anakinra chorda tympani cytokine epithelial Na+ channel feeding immune activation in vivo injured macrophage nerve injury neurophysiology neutrophil prevent receptor relating to nervous system response response to injury

项目摘要

Description (provided by applicant): Peripheral nerve injury has effects that extend beyond damaged neurons. However, the impact of injury on neighboring sensory fields is not well understood. We propose that immune cells, or "leukocytes", mediate changes in taste function. Macrophages respond to nerve injury, and extend to uninjured regions of the tongue. These leukocytes are predictive of normal neural taste responses. Neutrophils are also part of the immune response to injury, but they appear to have a negative effect on taste function. Neural injury alters sodium transduction in taste receptor cells, suggesting that the epithelial sodium channel (ENaC) is the site of functional plasticity. We will test the following hypotheses: (1) Neutrophils are the initial immune responders to gustatory nerve injury, and they induce deficits in taste function; (2) Nerve injury and leukocytes modulate ENaC expression and/or function; and (3) IL-12, a proinflammatory cytokine, maintains normal taste function after injury by promoting a balanced immune response. Resolution of these hypotheses will increase our understanding of dynamic immune responses to neural injury and their beneficial and harmful effects on sensory receptor cells. PUBLIC HEALTH RELEVANCE: The immune system plays an important role following neural injury, but its response to degeneration in the taste system is not well-understood. The proposed studies will determine the effects of an imbalanced immune response on taste function, and the mechanisms for immune-taste receptor cell interactions. Better understanding of the beneficial and harmful effects of the immune response to injury will lead to new strategies to promote normal sensory function.

描述（由申请人提供）：周围神经损伤的作用超出了受损的神经元。但是，受伤对邻近感觉场的影响尚不清楚。我们建议免疫细胞或“白细胞”介导味觉功能的变化。巨噬细胞对神经损伤做出反应，并延伸到舌头的未受伤区域。这些白细胞可预测正常的神经味道反应。中性粒细胞也是对损伤的免疫反应的一部分，但它们似乎对味觉功能产生负面影响。神经损伤改变了味觉受体细胞中的钠转导，表明上皮钠通道（ENAC）是功能可塑性的位置。我们将检验以下假设：（1）中性粒细胞是对味觉神经损伤的初始免疫反应者，它们会引起味觉功能的缺陷；（2）神经损伤和白细胞调节ENAC表达和/或功能；（3）促炎细胞因子IL-12通过促进均衡的免疫反应在受伤后保持正常的味觉功能。这些假设的解决将增加我们对神经损伤的动态免疫反应及其对感觉受体细胞的有益和有害影响的理解。公共卫生相关性：免疫系统在神经损伤后起着重要作用，但其对味觉系统的反应并不理解。拟议的研究将确定免疫反应不平衡的味觉功能的影响，以及免疫糖受体细胞相互作用的机制。更好地了解免疫反应对伤害的有益和有害影响将导致促进正常感觉功能的新策略。