权益分类	功能权益	普通用户	{{item.name}}会员
{{category.name}}	{{benefitItem.name}}

HIV-induced neuroinflammation associated with opiod abuse and tobacco smoke

艾滋病毒引起的与阿片类药物滥用和吸烟相关的神经炎症

基本信息

批准号：
9153336
负责人：
Yuri Persidsky
金额：
$ 73.35万
依托单位：
TEMPLE UNIV OF THE COMMONWEALTH
依托单位国家：
美国
项目类别：
财政年份：
2016
资助国家：
美国
起止时间：
2016-08-15 至 2021-05-31
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/9153336
关键词：
Acquired Immunodeficiency Syndrome Address Adhesions Affect Agonist Animals Antiviral Agents Atherosclerosis Blood - brain barrier anatomy Brain CCL2 gene CCR5 gene CXCR4 gene Cell Communication Cells Chronic Chronic Obstructive Airway Disease Clinic Competence Complex Data Depressed mood Deterioration Development Disease Drug abuse Encephalitis Endothelial Cells Endothelium Epidemic Exposure to Gene Expression HIV HIV Infections HIV-1 HIV-associated neurocognitive disorder Heroin Homing Immune Immune response Immunity In Vitro Infectious Agent Infiltration Inflammation Inflammatory Inflammatory Response Injury Intravenous Intravenous Drug Abuse Lead Leukocytes Link Lung Lung diseases Modeling Molecular Morphine Mus Natural Immunity Nerve Degeneration Neuronal Injury Opiates Opioid Organ Parasites Patients Pattern Pharmaceutical Preparations Pharmacotherapy Phenotype Population Predisposition Proteins Publishing Regulation Secondary to Smoke Smoker Smoking Structure of parenchyma of lung System Systemic disease Testing Time Tissues Tobacco Tobacco smoke Tobacco smoking Toxic effect Viremia Work acquired immunity adaptive immunity aryl hydrocarbons base brain endothelial cell brain tissue chemokine chemokine receptor clinically relevant cytokine drug abuser humanized mouse in vivo intravenous drug user macrophage migration monocyte monocyte chemoattractant protein 1 receptor mouse model neuroinflammation neuropathology neurotoxicity novel pre-clinical research public health relevance research study

项目摘要

DESCRIPTION (provided by applicant): Opiate drug abuse is a critical contributor to the global AIDS epidemic, and over a third of HIV infections in the U.S. can be linked to intravenous drug abuse. Recent estimates suggest that almost 20% of intravenous drug abusers are infected with HIV. Tobacco smoking is prevalent in HIV-infected patients, and is very common among intravenous drug abusers. Importantly, smoking is strongly associated with a number of non-AIDS conditions, including chronic obstructive lung disease (COPD), and this chronic inflammatory disease may contribute to the development of neuroinflammation associated with HIV infection. However, there is very little known about the combined effects of tobacco smoke and chronic opioid administration on the development of inflammatory responses, and even less known about the effects of these clinically relevant drugs on the development of neurodegeneration following HIV infection. We describe preliminary data which shows that the inflammatory response is both quantitatively and qualitatively distinct following the combination of tobacco and opiate administration. We propose to conduct experiments using humanized mice to examine the combined effects of chronic tobacco smoke exposure with and without chronic administration of morphine on the development of HIV-induced neuroinflammation. Our published and preliminary data show that the blood-brain barrier is a target for the effects of opiates and/or tobacco, as well as the inflammatory activity of monocytes and macrophages. We propose to investigate the mechanistic basis for the combined effects of these drug treatments on these cell populations. We believe the proposed studies will provide highly novel information about the effects of morphine and tobacco smoke on HIV-associated neurodegeneration in a clinically relevant immunological context.