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Woodsmoke-induced disruption of Nasal Microbiome and Cytokine Profiles

木烟引起的鼻微生物组和细胞因子谱的破坏

基本信息

批准号：
10196055
负责人：
Radhika Dhingra
金额：
$ 15.55万
依托单位：
UNIV OF NORTH CAROLINA CHAPEL HILL
依托单位国家：
美国
项目类别：
财政年份：
2021
资助国家：
美国
起止时间：
2021-04-01 至 2023-03-31
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/10196055
关键词：
Acute Address Air Pollutants Air Pollution Allergic Allergic rhinitis Antigens Asthma Bioinformatics Biological Response Modifiers Biomass Buffers Cause of Death Cells Cigarette Coronavirus Cross-Over Studies Data Disease Dose Ecosystem Electronic cigarette Enzyme-Linked Immunosorbent Assay Epidemiology Epithelial Cells Exposure to Feedback Foundations Future Homeostasis Host Defense Hour Immune Immune response Immune system Immunologics Incidence Individual Inflammation Inflammatory Influenza Inhalation Inhalation Exposure Intestinal Mucosa Knowledge Laboratories Lead Link Liquid substance Lung diseases Mediating Microbe Modeling Mucosal Immune Responses Mucositis Mucous Membrane Nasal Epithelium Nose Particulate Matter Pathway Analysis Placebos Population Predisposition Prevention Process Proteins Public Health Randomized Research Design Respiration Disorders Respiratory Mucosa Respiratory System Respiratory Tract Infections Role Sampling Signal Transduction Smoke Smoking Source Sputum Statistical Data Interpretation Structure of mucous membrane of nose System Time Tissues Viral Wildfire Work air filter ambient air pollution asthmatic beta diversity chemokine cigarette smoke commensal bacteria cytokine dysbiosis exposed human population gut microbiome host microbiota human subject immunoregulation influenzavirus microbial microbial colonization microbiome microbiota microorganism nasal microbiome novel particle particle exposure pathogen pollutant public health relevance resident commensals respiratory respiratory disease/disorder therapy respiratory health respiratory microbiome respiratory pathogen response sex therapy development wood smoke

项目摘要

ABSTRACT Global exposure to woodsmoke particles, primarily from wildfires and biomass burning, are an ever-increasing source of particulate matter, which is linked to many respiratory conditions. Successful defense against woodsmoke requires proficient immune regulation to maintain overall homeostasis. Critical to establishing an effective immune response to inhaled antigens, the nasal mucosa are known to be colonized by a large number of fungal, bacterial and viral micro- organisms. Disorders of the respiratory tract, however, are considered diseases of inflammation, not infection. Many studies have shown the role of commensal resident microbes and their metabolites in the initiation and/or progression of mucosal inflammation. For instance, incidence of allergic and inflammatory disease, including asthma and allergic rhinitis, is associated with a lack of diverse microbial colonization. Nasal cytokines are also known to be altered in those exposed to air pollutants (e.g., wildfire smoke), and to alter the robustness of response to viral insults, such as influenza and coronaviruses. Thus, we hypothesize that wood smoke exposure induces dysbiosis of the nasal microbiome and an altered inflammatory cytokine profile, which together have implications for respiratory health. We address this gap by identifying how concurrent microbiota and cytokine profiles change in response to exposure to woodsmoke. In this crossover study design, we will collect nasal epithelial lining fluid samples from healthy individuals at multiple time points post- exposure to either woodsmoke or filtered air in a controlled setting, in order to generate microbiome and the cytokine profiles. Once samples have been processed in the laboratory, we will conduct bioinformatic and statistical analyses to describe how acutely the microbiome and cytokines are concurrently altered in response to woodsmoke. We will also compare baseline profiles and responses in microbiome and cytokine responses by demographic and other factors. While we focus here on a woodsmoke exposure, this work has diverse applications including for future studies of atopic disease, ambient air pollution exposure, smoking; and potential development of therapies for respiratory disease.

摘要