Viral and allergen-driven immunity in chronic lung disease

慢性肺病中病毒和过敏原驱动的免疫

基本信息

  • 批准号:
    9886480
  • 负责人:
  • 金额:
    $ 68.49万
  • 依托单位:
  • 依托单位国家:
    美国
  • 项目类别:
  • 财政年份:
    2020
  • 资助国家:
    美国
  • 起止时间:
    2020-03-01 至 2027-01-31
  • 项目状态:
    未结题

项目摘要

Abstract Severe allergic asthmatic disease is characterized by significant airway structure changes and chronic inflammation predominated by eosinophils, mononuclear cells, and lymphocytes, and accompanied by mucus hypersecretion that depends upon the nature of the immune response. The most severe airways disease progresses through a continuum of responses ranging from manageable airway dysfunction to a steroid resistant state that is often a result of a severe exacerbation that is difficult to control. Over the more than 25 years of work in this area my laboratory has defined the role of numerous cytokines and chemokines that initiate and drive the pulmonary immune responses, identified innate immune molecules that shape the immune phenotype (TLRs, Notch), defined a role for respiratory viral infections that induce and exacerbate disease, examined epigenetic regulation of immune cell function, and more recently identified metabolic control of innate immune cell activation. Many of our previous discoveries have revealed potential therapeutic targets for pulmonary diseases, including studies in our 2nd NHLBI RO1 that examine stem cell factor and ILC2. One of our present NHLBI RO1 grants is examining the role of autophagy and cellular metabolism for innate immune cell function. Our most recent studies are addressing additional mechanisms linked to trained immunity within the lung, as well as development of lung responses that alter the structural and functional integrity of the lung. While we will be combining 2 RO1 with divergent themes, our overall objective of understanding how the pulmonary immune environment is developed and maintained during disease is central to all of our studies. Together, our past and ongoing investigations are revealing an integrated understanding of not only the immune responses during disease development, but also the long-term consequence of early disease and its relationship to altered lung function and development. Using this R35 mechanism, we will continue expanding on these areas of research that will be paradigm shifting. We will focus on specific goals including 1) determine how early RSV-induced responses in the lung alter the innate immune cell phenotype and induce lung structural changes that predisposes the lung to later allergic/asthmatic responses; 2) examine the role that stem cell factor (SCF) has on altering the activation of ILC2 populations in chronic pulmonary disease; and 3) investigate how cell metabolism alters immune cell development during disease to maintain and extend disease severity. Completion of these studies will provide new insights, establish new paradigms, and complete proof of concept studies needed to advance knowledge and validate new, therapeutically relevant mechanisms in clinical disease.
摘要

项目成果

期刊论文数量(0)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)

数据更新时间:{{ journalArticles.updateTime }}

{{ item.title }}
{{ item.translation_title }}
  • DOI:
    {{ item.doi }}
  • 发表时间:
    {{ item.publish_year }}
  • 期刊:
  • 影响因子:
    {{ item.factor }}
  • 作者:
    {{ item.authors }}
  • 通讯作者:
    {{ item.author }}

数据更新时间:{{ journalArticles.updateTime }}

{{ item.title }}
  • 作者:
    {{ item.author }}

数据更新时间:{{ monograph.updateTime }}

{{ item.title }}
  • 作者:
    {{ item.author }}

数据更新时间:{{ sciAawards.updateTime }}

{{ item.title }}
  • 作者:
    {{ item.author }}

数据更新时间:{{ conferencePapers.updateTime }}

{{ item.title }}
  • 作者:
    {{ item.author }}

数据更新时间:{{ patent.updateTime }}

Nicholas W Lukacs其他文献

Nicholas W Lukacs的其他文献

{{ item.title }}
{{ item.translation_title }}
  • DOI:
    {{ item.doi }}
  • 发表时间:
    {{ item.publish_year }}
  • 期刊:
  • 影响因子:
    {{ item.factor }}
  • 作者:
    {{ item.authors }}
  • 通讯作者:
    {{ item.author }}

{{ truncateString('Nicholas W Lukacs', 18)}}的其他基金

Viral and allergen-driven immunity in chronic lung disease
慢性肺病中病毒和过敏原驱动的免疫
  • 批准号:
    10347313
  • 财政年份:
    2020
  • 资助金额:
    $ 68.49万
  • 项目类别:
Viral and allergen-driven immunity in chronic lung disease
慢性肺病中病毒和过敏原驱动的免疫
  • 批准号:
    10551728
  • 财政年份:
    2020
  • 资助金额:
    $ 68.49万
  • 项目类别:
Autophagy regulation of RSV-induced pulmonary disease
RSV 诱导的肺部疾病的自噬调节
  • 批准号:
    8515518
  • 财政年份:
    2012
  • 资助金额:
    $ 68.49万
  • 项目类别:
Autophagy regulation of RSV-induced pulmonary disease
RSV 诱导的肺部疾病的自噬调节
  • 批准号:
    8340769
  • 财政年份:
    2012
  • 资助金额:
    $ 68.49万
  • 项目类别:
Project 4 Alteration of Mouse Maternal Gut Microbiota Alters Metabolic Profiles and Immune Phenotype in Offspring
项目 4 小鼠母体肠道微生物群的改变会改变后代的代谢特征和免疫表型
  • 批准号:
    10480058
  • 财政年份:
    2012
  • 资助金额:
    $ 68.49万
  • 项目类别:
Autophagy regulation of RSV-induced pulmonary disease
RSV 诱导的肺部疾病的自噬调节
  • 批准号:
    8687732
  • 财政年份:
    2012
  • 资助金额:
    $ 68.49万
  • 项目类别:
Autophagy regulation of RSV-induced pulmonary disease
RSV 诱导的肺部疾病的自噬调节
  • 批准号:
    8871569
  • 财政年份:
    2012
  • 资助金额:
    $ 68.49万
  • 项目类别:
TLR and Notch Ligand in RSV-induced Disease
RSV 诱导疾病中的 TLR 和 Notch 配体
  • 批准号:
    7878285
  • 财政年份:
    2009
  • 资助金额:
    $ 68.49万
  • 项目类别:
The Role of C-C Chemokines in Eosinophil Airway Inflammation
C-C 趋化因子在嗜酸性粒细胞气道炎症中的作用
  • 批准号:
    7846595
  • 财政年份:
    2009
  • 资助金额:
    $ 68.49万
  • 项目类别:
TLR and Notch Ligand in RSV-induced Disease
RSV 诱导疾病中的 TLR 和 Notch 配体
  • 批准号:
    8206794
  • 财政年份:
    2008
  • 资助金额:
    $ 68.49万
  • 项目类别:

相似海外基金

EXposomic Profiling in Airway disease to uNravel Determinants of disease in Asthma (EXPAND-Asthma) Center
气道疾病暴露组分析以解开哮喘疾病的决定因素 (EXPAND-Asthma) 中心
  • 批准号:
    10744673
  • 财政年份:
    2023
  • 资助金额:
    $ 68.49万
  • 项目类别:
Bacteriophage as a predictive biomarker in chronic Pseudomonas airway disease
噬菌体作为慢性假单胞菌气道疾病的预测生物标志物
  • 批准号:
    10723956
  • 财政年份:
    2023
  • 资助金额:
    $ 68.49万
  • 项目类别:
Defining a gene expression signature of airway disease, COPD exacerbations, and response to treatment
定义气道疾病、COPD 恶化和治疗反应的基因表达特征
  • 批准号:
    10733573
  • 财政年份:
    2023
  • 资助金额:
    $ 68.49万
  • 项目类别:
Impact of Maternal Arsenic Exposure on Offspring's Epigenetic Reprogramming of Allergic Airway Disease
母亲砷暴露对后代过敏性气道疾病表观遗传重编程的影响
  • 批准号:
    10733607
  • 财政年份:
    2023
  • 资助金额:
    $ 68.49万
  • 项目类别:
Hydrogen Sulfide in Neonatal Airway Disease
新生儿气道疾病中的硫化氢
  • 批准号:
    10603293
  • 财政年份:
    2023
  • 资助金额:
    $ 68.49万
  • 项目类别:
Immune Mediators of IL-22 Signaling Alter Allergic Airway Disease
IL-22 信号的免疫介质改变过敏性气道疾病
  • 批准号:
    10853347
  • 财政年份:
    2023
  • 资助金额:
    $ 68.49万
  • 项目类别:
The role of anaerobic microbiota in cystic fibrosis airway disease trajectory
厌氧微生物群在囊性纤维化气道疾病轨迹中的作用
  • 批准号:
    10716654
  • 财政年份:
    2023
  • 资助金额:
    $ 68.49万
  • 项目类别:
Microbial adaptation of Pseudomonas lipid A structure in CF airway disease progress
假单胞菌脂质 A 结构在 CF 气道疾病进展中的微生物适应
  • 批准号:
    10722599
  • 财政年份:
    2023
  • 资助金额:
    $ 68.49万
  • 项目类别:
The role of anaerobic microbiota in cystic fibrosis airway disease trajectory
厌氧微生物群在囊性纤维化气道疾病轨迹中的作用
  • 批准号:
    10985906
  • 财政年份:
    2023
  • 资助金额:
    $ 68.49万
  • 项目类别:
Mentoring patient-oriented researchers in inflammatory airway disease
指导炎症性气道疾病领域以患者为中心的研究人员
  • 批准号:
    10657746
  • 财政年份:
    2022
  • 资助金额:
    $ 68.49万
  • 项目类别:
{{ showInfoDetail.title }}

作者:{{ showInfoDetail.author }}

知道了