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受压力的节肢动物:病原体-媒介界面的应激反应与免疫

Arthropods Under Pressure: Stress Responses and Immunity at the Pathogen-Vector Interface.

作者信息

Rosche Kristin L, Sidak-Loftis Lindsay C, Hurtado Joanna, Fisk Elizabeth A, Shaw Dana K

机构信息

Program in Vector-borne Disease, Department of Veterinary Microbiology and Pathology, Washington State University, Pullman, WA, United States.

出版信息

Front Immunol. 2021 Feb 15;11:629777. doi: 10.3389/fimmu.2020.629777. eCollection 2020.

Abstract

Understanding what influences the ability of some arthropods to harbor and transmit pathogens may be key for controlling the spread of vector-borne diseases. Arthropod immunity has a central role in dictating vector competence for pathogen acquisition and transmission. Microbial infection elicits immune responses and imparts stress on the host by causing physical damage and nutrient deprivation, which triggers evolutionarily conserved stress response pathways aimed at restoring cellular homeostasis. Recent studies increasingly recognize that eukaryotic stress responses and innate immunity are closely intertwined. Herein, we describe two well-characterized and evolutionarily conserved mechanisms, the Unfolded Protein Response (UPR) and the Integrated Stress Response (ISR), and examine evidence that these stress responses impact immune signaling. We then describe how multiple pathogens, including vector-borne microbes, interface with stress responses in mammals. Owing to the well-conserved nature of the UPR and ISR, we speculate that similar mechanisms may be occurring in arthropod vectors and ultimately impacting vector competence. We conclude this Perspective by positing that novel insights into vector competence will emerge when considering that stress-signaling pathways may be influencing the arthropod immune network.

摘要

了解哪些因素会影响某些节肢动物携带和传播病原体的能力,可能是控制媒介传播疾病传播的关键。节肢动物免疫在决定病原体获取和传播的媒介能力方面起着核心作用。微生物感染会引发免疫反应,并通过造成身体损伤和营养剥夺对宿主施加压力,从而触发旨在恢复细胞内稳态的进化保守应激反应途径。最近的研究越来越认识到真核生物应激反应和先天免疫紧密相连。在此,我们描述两种特征明确且进化保守的机制,即未折叠蛋白反应(UPR)和综合应激反应(ISR),并研究这些应激反应影响免疫信号传导的证据。然后我们描述包括媒介传播微生物在内的多种病原体如何与哺乳动物的应激反应相互作用。由于UPR和ISR具有高度保守的特性,我们推测类似的机制可能在节肢动物媒介中发生,并最终影响媒介能力。我们在本观点文章结尾提出,当考虑到应激信号通路可能正在影响节肢动物免疫网络时,将会出现关于媒介能力的新见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/24dc/7917218/5f7b1bf4b1a5/fimmu-11-629777-g001.jpg

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