Lung inflammation is central to the most lung diseases which include pneumonia, bronchitis, asthma, fibrosis and emphysema. Understanding the molecular mechanisms underlying these diseases is critical to our future success in developing new treatment strategies. This NRSA competitive renewal is designed to bring new basic and clinical medical scientists together to study in a research intensive environment with the goal of generating the next generation of investigators working to understand, prevent and treat lung disease. This T32 utilizes the infrastructure of the Ohio State University's Davis Heart and Lung Research Institute, the OSU Pulmonary Allergy Critical Care and Sleep Medicine Division, the Center for Microbial Interface Biology and the training programs of the OSU NIH Center for Translational Sciences Award to provide the training platforms. We have formed a training faculty with broad backgrounds to support specific experience opportunities in lung host defense, apoptosis injury and repair, molecular genetics, cell signaling, and translational medicine. Our plan is to recruit 2 postdoctoral Ph.D. and 2 M.D. trainees at a time into a 2 year program that provides an innovative experience that breeds interdisciplinary understanding and links these trainees with both junior and senior faculty in an intensive and creative environment that promotes future research careers in lung disease. Specifically the objectives of the program are fourfold. Objective 1. To provide sufficient didacti, interactive and technical background in molecular biology, immunology, cell signaling, proteomics and functional genomics to allow trainees to be able to move easily between these disciplines and to be able to translate their knowledge into further understanding of the origins o pulmonary disease. Objective 2. To develop an innovative program which ensures that trainees move rapidly into laboratory experiences that are likely to be successful. Furthermore, by using peer review and interdisciplinary faculty oversight, we will instill in the trainees a consistent momentum and focus on their chosen research topics throughout the training period. Objective 3. To immerse the trainees in a creative environment and positive research atmosphere which ensures the greatest possibility for success and retention in the ranks of scientific investigators and teachers. In addition, specific training will be provided in the ethics and philosophy of research with the intent of producing scientists who will operate at the highest levels of intellectual integrity. Objective 4. To develop long-range programs which encourage women and minorities to pursue careers in pulmonary science and research and more importantly, to build sufficient infrastructure and support systems within the training program to ensure the success of the motivated trainee.

Public Health Relevance

Inflammatory lung disease is central to most disorders of the lung. This proposal builds an infrastructure to provide training for scientists in the mechanisms underlying these lung diseases that include asthma, pneumonia, emphysema, acute lung failure and lung fibrosis. It links a vibrant faculty from the Davis Heart and Lung Institute with institutional support to train M.D. and Ph.D. scientists in an interdisciplinary environment.

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Institutional National Research Service Award (T32)
Project #
5T32HL007946-14
Application #
8878324
Study Section
NHLBI Institutional Training Mechanism Review Committee (NITM)
Program Officer
Colombini-Hatch, Sandra
Project Start
2000-09-30
Project End
2016-06-30
Budget Start
2015-07-01
Budget End
2016-06-30
Support Year
14
Fiscal Year
2015
Total Cost
Indirect Cost
Name
Ohio State University
Department
Internal Medicine/Medicine
Type
Schools of Medicine
DUNS #
832127323
City
Columbus
State
OH
Country
United States
Zip Code
43210
Arnett, Eusondia; Weaver, Ashlee M; Woodyard, Kiersten C et al. (2018) PPAR? is critical for Mycobacterium tuberculosis induction of Mcl-1 and limitation of human macrophage apoptosis. PLoS Pathog 14:e1007100
Locke, Landon W; Kothandaraman, Shankaran; Tweedle, Michael et al. (2018) Use of a leukocyte-targeted peptide probe as a potential tracer for imaging the tuberculosis granuloma. Tuberculosis (Edinb) 108:201-210
Le, Van; Crouser, Elliott D (2018) Potential immunotherapies for sarcoidosis. Expert Opin Biol Ther 18:399-407
Jones, Christopher J; Wozniak, Daniel J (2017) Psl Produced by Mucoid Pseudomonas aeruginosa Contributes to the Establishment of Biofilms and Immune Evasion. MBio 8:
Pyle, Charlie J; Azad, Abul K; Papp, Audrey C et al. (2017) Elemental Ingredients in the Macrophage Cocktail: Role of ZIP8 in Host Response to Mycobacterium tuberculosis. Int J Mol Sci 18:
Fatehchand, Kavin; McMichael, Elizabeth L; Reader, Brenda F et al. (2016) Interferon-? Promotes Antibody-mediated Fratricide of Acute Myeloid Leukemia Cells. J Biol Chem 291:25656-25666
Barger, Jennifer F; Rahman, Mohammad A; Jackson, Devine et al. (2016) Extracellular miRNAs as biomarkers in cancer. Food Chem Toxicol 98:66-72
Gautam, Shalini; Fatehchand, Kavin; Elavazhagan, Saranya et al. (2016) Reprogramming Nurse-like Cells with Interferon ? to Interrupt Chronic Lymphocytic Leukemia Cell Survival. J Biol Chem 291:14356-62
Ren, Li; Campbell, Amanda; Fang, Huiqing et al. (2016) Analysis of the Effects of the Bruton's tyrosine kinase (Btk) Inhibitor Ibrutinib on Monocyte Fc? Receptor (Fc?R) Function. J Biol Chem 291:3043-52
Elavazhagan, Saranya; Fatehchand, Kavin; Santhanam, Vikram et al. (2015) Granzyme B expression is enhanced in human monocytes by TLR8 agonists and contributes to antibody-dependent cellular cytotoxicity. J Immunol 194:2786-95

Showing the most recent 10 out of 30 publications