Widespread Anticoagulant Poison Exposure is Linked with Immune Dysregulation and Severe Notoedric Mange in Urban Bobcats
Widespread Anticoagulant Poison Exposure is Linked with Immune Dysregulation and Severe Notoedric Mange in Urban Bobcats
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城市山猫广泛的抗凝剂中毒与免疫失调和严重的疥疮有关
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发表时间：
2018
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通讯作者：
R. Wayne
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作者：
Laurel E. K. Serieys;A. Lea;M. Epeldegui;J. Foley;J. Moriarty;S. Riley;C. Uittenbogaart;Devaughn L. Fraser;A. Mouton;R. Wayne
作者：Laurel E. K. 系列；莉亚，阿曼达；玛尔塔·埃佩尔德吉；弗利，珍妮特；莫里亚蒂，乔安妮·盖尔；莱利，赛斯 P.D.；克里斯特尔·H·乌滕博加特；弗雷泽，德沃恩；木桐，爱丽丝；韦恩，罗伯特·K. |摘要：人类活动通过各种新的压力源威胁野生动物，例如接触有毒物质。抗凝血灭鼠剂 (AR) 是一种在世界范围内使用的有毒物质，通过生物蓄积，威胁捕食有毒啮齿动物或其天敌的物种。我们研究了南加州城市山猫的数量，由于疥癣，它们的数量从 2002 年到 2005 年迅速下降。我们首先使用人群的血液和肝脏样本评估了 AR 暴露的流行率，并发现了广泛的暴露 (g90%)。与疥疮相关的死亡与累积的第一代和第二代 AR 暴露密切相关。这些发现表明，接触第一代和第二代 AR 是导致该疾病的根本原因。我们接下来的目标是了解 AR 暴露对该自然群体的亚致死免疫学和生理学影响。我们使用了两种方法：1）我们使用了一套全面的健康检测（全血细胞计数、血液化学评估和免疫学分析），2）我们量化了一部分个体血液中 AR 诱导的差异基因表达。我们发现，亚致死的 AR 暴露（主要通过敌鼠酮暴露来测量）与全身性炎症的标志性指标相关，这种炎症持续存在可能会促进免疫功能障碍。此外，差异基因表达的发现支持了免疫学分析的结果。此外，与上皮维持相关的基因表达的减少同时与外寄生免疫反应相关的基因表达的减少可能解释了 AR 暴露与疥疮易感性之间的联系。亚致死暴露的这种间接影响体现了在人类主导的环境中保护野生种群免受常见有毒物质侵害的挑战。
Author(s): Serieys, Laurel E. K.; Lea, Amanda; Epeldegui, Marta; Foley, Janet; Moriarty, Joanne Gale; Riley, Seth P. D.; Uittenbogaart, Christel H.; Fraser, Devaughn; Mouton, Alice; Wayne, Robert K. | Abstract: Human activities threaten wildlife with a variety of novel stressors such as exposure to toxicants. Anticoagulant rodenticides (ARs) are toxicants applied worldwide and through bioaccumulation, threaten species that prey on poisoned rodents or their predators. We studied a population of urban bobcats in southern California that declined rapidly from 2002-2005 due to notoedric mange. We first assessed prevalence of AR exposure using blood and liver samples across the population and found widespread exposure (g90%). Death associated with mange was strongly correlated with cumulative first- and second-generation AR exposure. These findings suggested that exposure to both first- and second-generation ARs were an underlying cause of the disease. We next aimed to understand the sublethal immunological and physiological effects of AR exposure in this natural population. We used two approaches: 1) we used a comprehensive suite of health assays (complete blood counts, blood chemistry assessment, and immunological profiling), and 2) we quantified AR-induced differential gene expression in blood for a subset of individuals. We found that sublethal AR exposure, primarily measured as exposure to diphacinone, is associated with hallmark indicators of generalized systemic inflammation that in persistence could promote immune dysfunction. Further, differential gene expression findings supported the results of immunological profiling. Further, a decrease in the expression of genes associated with epithelial maintenance simultaneous to a decrease in gene expression linked with ectoparasitic immune response may explain the link between AR exposure and mange vulnerability. Such indirect effects of sublethal exposure exemplify the challenge of protecting wild populations from common toxicants in human-dominated environments.