This application requests support to continue a highly successful SCOR in Occupational and Immunologic Lung Disease at the University of Iowa. The overall goal of the Occupational and Immunologic Lung Disease SCOR Program at Iowa is to perform coordinated interdisciplinary research aimed at elucidating the basic mechanisms for the development of disease in these disorders. A related goal of the SCOR Program is to determine if information obtained from these basic studies improves the care of patients with Occupational and Immunologic Lung Disease. The basic and clinical studies that were chosen for the renewal of this program are highly interactive and the success of each of the projects will be significantly enhanced by the interactions within the SCOR Program. There are six projects and four cores in the program. Project I (Determinants of the Disease Activity and Prognosis for Interstitial Lung Disease) is the clinical project which will determine factors which predict prognosis in patients with sarcoidosis, asbestosis, idiopathic pulmonary fibrosis, and interstitial lung disease associated with Rheumatoid arthritis. Projects VI-X (VI: Regulation of PGH Synthase in alveolar Macrophages from Normal Individuals and Cigarette Smokers; VII: Inflammatory Effects of PMN Metabolites of Linoleic Acid; VIII: Interaction of Latent Viral Genes with Cell-Derived Cytokine Genes; IX: Human Cytomegalovirus Immediate Early Gene Expression in Inflammatory Cells of the Human Lung and Their Effects on Promoters; and X: Post-transcriptional Regulation, Processing and Secretion of Interleukin-I) are basic studies which evaluate various aspects of the pathophysiology of these disorders. Acquisition of new information from these studies should enhance our disorders. The six projects in the Occupational and Immunologic Lung Disease SCOR will be supported by four core facilities: Administration, Biometry, Clinical, and Pathology. The research team consists of investigators from the University of Iowa College of Medicine and the University of British Columbia (Vancouver, B.C., Canada), Departments of Medicine, Microbiology, Biochemistry, Pediatrics, Radiology, Physiology, Pathology, and Preventive Medicine/Biostatistics. Essentially all of these investigators have interacted closely in research projects for some time.

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Specialized Center (P50)
Project #
2P50HL037121-06
Application #
3106800
Study Section
Special Emphasis Panel (SRC (MA))
Project Start
1986-12-01
Project End
1996-11-30
Budget Start
1992-02-07
Budget End
1992-11-30
Support Year
6
Fiscal Year
1992
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
Monick, M M; Carter, A B; Gudmundsson, G et al. (1999) A phosphatidylcholine-specific phospholipase C regulates activation of p42/44 mitogen-activated protein kinases in lipopolysaccharide-stimulated human alveolar macrophages. J Immunol 162:3005-12
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
Carter, A B; Monick, M M; Hunninghake, G W (1998) Lipopolysaccharide-induced NF-kappaB activation and cytokine release in human alveolar macrophages is PKC-independent and TK- and PC-PLC-dependent. Am J Respir Cell Mol Biol 18:384-91

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