Dual Role for Innate Lymphoid Cells in Pathogenesis of Brucellosis

先天淋巴细胞在布鲁氏菌病发病机制中的双重作用

• 批准号: 10027505
• 负责人: Jerod Skyberg
• 金额: $ 22.62万
• 依托单位: UNIVERSITY OF MISSOURI-COLUMBIA
• 依托单位国家: 美国
• 财政年份: 2020
• 资助国家: 美国
• 起止时间: 2020-06-19 至 2022-05-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/10027505
• 关键词: Adoptive Transfer; B-Lymphocytes; Bacterial Infections; Biological Assay; Brucella; Brucellosis; CASP1 gene; Cell physiology; Cells; Coculture Techniques; Data; Disease; Gastrointestinal tract structure; Goals; Human; Immune; Infection; Infection Control; Inflammasome; Inflammation; Interferon Type II; Joints; Kinetics; Lung; Lung infections; Lymphoid Cell; Mediating; Mouse Strains; Mucous Membrane; Mus; NOS2A gene; Nitric Oxide; Outcome; Pathogenesis; Play; Predisposition; Production; Publishing; Role; Route; Source; Spleen; Symptoms; T-Lymphocyte; Testing; Time; Tissues; Wild Type Mouse; Zoonoses; adaptive immunity; body system; cytokine; immunoregulation; in vivo; macrophage; mortality; mucosal site; neglect; oral infection; response

Project Summary/Abstract: Brucella infection causes a myriad of symptoms due to the ability of Brucella to infect almost any organ or organ system. Innate lymphoid cells are abundant in mucosal tissues which serve as a portal of entry for Brucella infection, and we have found that innate lymphoid cells regulate both inflammation and control of Brucella infection. In this proposal, we will investigate interactions between innate lymphoid cells and inflammasomes to determine how innate lymphoid cells from different tissues regulate Brucella-induced inflammation. We will also determine the relative contribution of different innate lymphoid cell subsets to controlling inflammation and Brucella infection. Collectively the results of our study will enhance our understanding of how Brucella is able to utilize mucosal sites as a portal of infection and cause inflammation within different host tissues.

项目摘要/摘要： 布鲁氏菌感染引起了无数症状，因为布鲁氏菌能够感染几乎 任何器官或器官系统。先天淋巴样细胞在粘膜组织中丰富 作为布鲁氏菌感染的入口门户，我们发现先天淋巴样细胞调节 布鲁氏菌感染的炎症和控制。在此提案中，我们将调查互动 在先天淋巴样细胞和炎症中，以确定先天淋巴样细胞如何 不同的组织调节布鲁氏菌引起的炎症。我们还将确定亲戚 不同先天淋巴样细胞亚群对控制炎症和布鲁氏菌的贡献 感染。总体而言，我们的研究结果将增强我们对布鲁氏菌的理解 能够利用粘膜部位作为感染的门户，并在不同宿主内引起炎症 组织。