The overall goal of the Occupational and Immunologic Lung Disease SCOR Program at the University of Iowa is to perform coordinated interdisciplinary research aimed at elucidating the basic mechanisms responsible for the development of these disorders. A related goal of the Occupational and Immunologic Lung Disease SCOR Program is to determine if information obtained from these basic studies improves the care of patients with these disorders. Bronchoalveolar lavage which obtains inflammatory and immune effector cells from the lung is an important technique for both types of studies. Project I (Bronchoalveolar Lavage and Interstitial Lung Disease) is a clinical study which evaluates the clinical use of bronchoalveolar lavage in selected interstitial lung disorders. Projects II-V (II: Local Immune Response at Sites of Disease in Sarcoidosis; III: Transport of Immunoglobulin Proteins in the Lung; IV: Epidemiology and Pulmonary Responses to Organic Dust Exposure; and V: Specific Cellular Mechanisms in a Rat Model of Hypersensitivity Pneumonitis) are basic studies which evaluate the epidemiology and pathophysiology of various occupational and immunologic lung diseases. Acquisition of new information from these studies should enhance our understanding of the pathogenesis and improve our care of patients with these disorders. The five projects in the Occupational and Immunologic Lung Disease SCOR will be supported by two core facilities: an Administrative Core and a Biometry Core.

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Specialized Center (P50)
Project #
5P50HL037121-03
Application #
3106802
Study Section
(SRC)
Project Start
1986-12-01
Project End
1991-11-30
Budget Start
1988-12-01
Budget End
1989-11-30
Support Year
3
Fiscal Year
1989
Total Cost
Indirect Cost
Name
University of Iowa
Department
Type
Schools of Medicine
DUNS #
041294109
City
Iowa City
State
IA
Country
United States
Zip Code
52242
Yarovinsky, Timur O; Monick, Martha M; Hunninghake, Gary W (2003) Integrin receptors are crucial for the restimulation of activated T lymphocytes. Am J Respir Cell Mol Biol 28:607-15
Yarovinsky, T O; Hunninghake, G W (2001) Lung fibroblasts inhibit activation-induced death of T cells through PGE(2)-dependent mechanisms. Am J Physiol Lung Cell Mol Physiol 281:L1248-56
Chen, W; Hunninghake, G W (2000) Effects of ragweed and Th-2 cytokines on the secretion of IL-8 in human airway epithelial cells. Exp Lung Res 26:229-39
Geist, L J; Powers, L S; Monick, M M et al. (2000) Asbestos stimulation triggers differential cytokine release from human monocytes and alveolar macrophages. Exp Lung Res 26:41-56
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Gudmundsson, G; Hunninghake, G W (1999) Respiratory epithelial cells release interleukin-8 in response to a thermophilic bacteria that causes hypersensitivity pneumonitis. Exp Lung Res 25:217-28
Carter, A B; Monick, M M; Hunninghake, G W (1999) Both Erk and p38 kinases are necessary for cytokine gene transcription. Am J Respir Cell Mol Biol 20:751-8
Monick, M M; Carter, A B; Hunninghake, G W (1999) Human alveolar macrophages are markedly deficient in REF-1 and AP-1 DNA binding activity. J Biol Chem 274:18075-80
Gudmundsson, G; Monick, M M; Hunninghake, G W (1999) Viral infection modulates expression of hypersensitivity pneumonitis. J Immunol 162:7397-401
Goebel, E A; Davidson, B L; Graham, S M et al. (1998) Tumor reduction in vivo after adenoviral mediated gene transfer of the herpes simplex virus thymidine kinase gene and ganciclovir treatment in human head and neck squamous cell carcinoma. Otolaryngol Head Neck Surg 119:331-6

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