基本信息
浏览量:2
职业迁徙
个人简介
My Research
KEYWORDS
lung diseases associated with environmental pollutants: asthma, chronic inflammation, airway and arterial remodeling, interactions between the immune system and environmental pollutants, Soluble mediators (cytokines such as IL-13, IL-10 family cytokines)
SUMMARY
Exposure to airborne pollutants and cigarette smoke are major causes of chronic inflammation in the lungs. The lungs also become more susceptible to infection with viruses or bacteria. The result is the dysfunction of the bronchi that transport air to and from the alveoli, and to the blood vessels that circulate the blood through the lungs. The major focus point of research in the laboratory is to define the role of secreted proteins by which immune cells communicate with the cells that make up the structure of the lungs. This research has identified one of these mediators, called Interleukin-13 (IL-13), to directly initiate the processes that induce the cardinal signs of asthma: bronchial constriction, inflammation and increased mucus production. At the present time, we have a grant from the National Institute of Health that has the goal to help to develop a drug that inhibits Interleukin-13 and a few other key mediators of asthma. We have most recently begun to investigate the blood vessels in the lungs. We have shown for the first time experimentally that the immune response can induce severe wall-thickening of arteries (structure stained in brown by labeling with a smooth muscle specific antibody) in the lungs. In addition, the studies showed that Interleukin-13 (IL-13) is a critical, indirect communicator in the process that leads to the severe thickening of the pulmonary arterial walls. This thickening of the pulmonary arterial walls has been described in patients who have pulmonary hypertension, a debilitating disease that frequently accompanies chronic lung disease caused by smoking. This research might aid in developing new methods to follow disease progression and tailor treatment strategies in patients with pulmonary hypertension.
KEYWORDS
lung diseases associated with environmental pollutants: asthma, chronic inflammation, airway and arterial remodeling, interactions between the immune system and environmental pollutants, Soluble mediators (cytokines such as IL-13, IL-10 family cytokines)
SUMMARY
Exposure to airborne pollutants and cigarette smoke are major causes of chronic inflammation in the lungs. The lungs also become more susceptible to infection with viruses or bacteria. The result is the dysfunction of the bronchi that transport air to and from the alveoli, and to the blood vessels that circulate the blood through the lungs. The major focus point of research in the laboratory is to define the role of secreted proteins by which immune cells communicate with the cells that make up the structure of the lungs. This research has identified one of these mediators, called Interleukin-13 (IL-13), to directly initiate the processes that induce the cardinal signs of asthma: bronchial constriction, inflammation and increased mucus production. At the present time, we have a grant from the National Institute of Health that has the goal to help to develop a drug that inhibits Interleukin-13 and a few other key mediators of asthma. We have most recently begun to investigate the blood vessels in the lungs. We have shown for the first time experimentally that the immune response can induce severe wall-thickening of arteries (structure stained in brown by labeling with a smooth muscle specific antibody) in the lungs. In addition, the studies showed that Interleukin-13 (IL-13) is a critical, indirect communicator in the process that leads to the severe thickening of the pulmonary arterial walls. This thickening of the pulmonary arterial walls has been described in patients who have pulmonary hypertension, a debilitating disease that frequently accompanies chronic lung disease caused by smoking. This research might aid in developing new methods to follow disease progression and tailor treatment strategies in patients with pulmonary hypertension.
研究兴趣
论文共 144 篇作者统计合作学者相似作者
按年份排序按引用量排序主题筛选期刊级别筛选合作者筛选合作机构筛选
时间
引用量
主题
期刊级别
合作者
合作机构
Gastro Hep Advancesno. 4 (2023): 608-620
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINEno. 9 (2023): 538-538
引用1浏览0引用
1
0
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE (2023)
引用0浏览0引用
0
0
Arthritis & rheumatology (Hoboken, N.J.)no. 12 (2023): 2240-2251
B. E. Funke,J. G. Terry,S. Nair,J. Carr, H. Nian, B. Borlaug, S. C. Erzurum, R. P. Frantz,G. Grunig,P. M. Hassoun, E. Horn, M. S. Jacob,
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE (2023)
引用0浏览0引用
0
0
Rachel Lam, James Kim, Mihika Ramprasad, Urooj Javed,Sanjiti Podury,Sophia Kwon,George Crowley,Theresa Schwartz,Rachel Zeig-Owens,David J. Prezant,Gabriele Grunig,Anna Nolan
CHESTno. 4 (2023): 5111A-5112A
加载更多
作者统计
合作学者
合作机构
D-Core
- 合作者
- 学生
- 导师
数据免责声明
页面数据均来自互联网公开来源、合作出版商和通过AI技术自动分析结果,我们不对页面数据的有效性、准确性、正确性、可靠性、完整性和及时性做出任何承诺和保证。若有疑问,可以通过电子邮件方式联系我们:report@aminer.cn