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2000 Progress Report: Multi-component Intervention Study of Asthma in Children from Rural Communities
EPA Grant Number: R826711C002Subproject: this is subproject number 002 , established and managed by the Center Director under grant R826711
(EPA does not fund or establish subprojects; EPA awards and manages the overall grant for this center).
Center: University of Iowa Children's Environmental Airway Disease Center
Center Director: Hunninghake, Gary W.
Title: Multi-component Intervention Study of Asthma in Children from Rural Communities
Investigators: Schwartz, David , Chrischilles, Elizabeth , Hunninghake, Gary W. , Nauseef, William
Current Investigators: Chrischilles, Elizabeth , Hunninghake, Gary W. , Merchant, James A. , Schwartz, David
Institution: University of Iowa
EPA Project Officer: Fields, Nigel
Project Period: January 1, 1998 through January 1, 2002
Project Period Covered by this Report: January 1, 1999 through January 1, 2000
Project Amount: Refer to main center abstract for funding details.
RFA: Centers for Children's Environmental Health and Disease Prevention Research (1998)
Research Category: Children's Health , Health Effects
Description:
Objective:The theme of this program is to investigate the etiology and pathogenesis of airway disease in children from rural communities. Progress Summary:
The program's progress is reported below by project:
Project 1:
Multicomponent Intervention Study of Asthma in Children from Rural
Communities: the Rural Health Study
PI: Elizabeth Chrischilles, Ph.D.
The most significant achievement during the past year has been the development of a specific protocol for the multi-component intervention and for the assessment of its effect. To date, no protocol is available for a community-based intervention encompassing both environmental and medical issues related to asthma care in a rural environment, particularly with focus on individualized family counseling related to barriers for asthma care. The most important aspect of the study is that we have a 90 percent response rate.
Project 2:
A Model to Study the Development of Persistent Environmental Airway
Disease
PI: David A. Schwartz, M.D., M.P.H. (Duke University)
The investigators have found that subacute exposure to grain dust caused chronic airway lesions that are associated with airway hyperreactivity and airway remodeling. Moreover, the development of chronic grain dust induced airway disease appears to be mediated by endotoxin, because mice genetically hyporesponsive to endotoxin do not develop chronic grain dust induced airway disease.
Project 3:
Mechanisms That Initiate, Promote and Resolve Grain Dust Induced
Inflammation
PI: William Nauseef, M.D.
Studies related to the pathophysiology of asthma commonly involve either in vivo human and animal systems or in vitro systems with single cell types. Although both of these approaches provide crucially important insights, it often is difficult to bridge the knowledge that the two systems provide. We are developing co-culture systems that will allow us to explore the complex interactions between airway cells that are the basis for the inflammatory response to grain dust. We have found that the response to grain dust is very cell specific.
Project 4:
Role of RSV Infection and Endotoxin in Airway Inflammation
PI: Gary
W. Hunninghake, M.D.
RSV upregulates the p45 ERK kinase and then this is related to IL-8 production by airway epithelium. These investigators also observed that TH-1 and TH-2 cytokines regulate IL-8 release by airway epithelium. Importantly, we found that environmental exposures may increase replication of viruses in the airways.
Future Activities:All of the projects are progressing according to the timeline specified in the original proposal. There has been on changes in the direction of the work or the schedule.
Journal Articles on this Report: 9 Displayed | Download in RIS Format
| Other subproject views: | All 11 publications | 10 publications in selected types | All 10 journal articles |
| Other center views: | All 33 publications | 32 publications in selected types | All 32 journal articles |
| Type | Citation | ||
|---|---|---|---|
|
|
Arbour NC, Lorenz E, Schutte BC, Zabner J, Kline JN, Jones M, Frees K, Watt JL, Schwartz DA. TLR4 mutations are associated with endotoxin hyporesponsiveness in humans. Nature Genetics 2000;25(2):187-191. |
R826711 (Final) R826711C001 (2000) R826711C002 (2000) R826711C004 (Final) |
not available |
|
|
George CL, Jin H, Wohlford-Lenane CL, O’Neill ME, Phipps JC, O’Shaughnessy P, Kline JN, Thorne PS, Schwartz DA. Endotoxin responsiveness and subchronic grain dust-induced airway disease. American Journal of Physiology-Lung Cellular and Molecular Biology 2001;280(2):L203-L213. |
R826711 (Final) R826711C001 (2000) R826711C002 (2000) R826711C004 (Final) |
not available |
|
|
Kline JN, Jagielo PJ, Watt JL, Schwartz DA. Bronchial hyperreactivity is associated with enhanced grain dust-induced airflow obstruction. Journal of Applied Physiology 2000;89(3):1172-1178. |
R826711 (Final) R826711C001 (2000) R826711C002 (2000) R826711C004 (Final) |
not available |
|
|
Kline JN, Cowden JD, Hunninghake GW, Watt JL, Wohlford-Lenane CL, Powers LS, Jones MP, Schwartz DA. Variable airway responsiveness to inhaled lipopolysaccharide. American Journal of Respiratory and Critical Care Medicine 1999;160(1):297-303, 1999. |
R826711C001 (2000) R826711C002 (2000) |
not available |
|
|
Moreland JG, Fuhrman RM, Wohlford-Lenane CL, Quinn TJ, Benda E, Pruessner JA, Schwartz DA. TNF-α and IL-1β are not essential to the inflammatory response in LPS -induced airway disease. American Journal of Physiology-Lung Cellular and Molecular Biology 2001;280(1):L173-L180. |
R826711 (Final) R826711C001 (2000) R826711C002 (2000) R826711C004 (Final) |
not available |
|
|
Quinn TJ, Taylor S, Wohlford-Lenane CL, Schwartz DA. IL-10 reduces grain dust-induced airway inflammation and airway hyperreactivity. Journal of Applied Physiology 2000;88(1):173-179. |
R826711 (Final) R826711C001 (2000) R826711C002 (2000) R826711C004 (Final) |
not available |
|
|
Schwartz DA, Wohlford-Lenane CL, Quinn TJ, Krieg AM. Bacterial DNA or oligonucleotides containing unmethylated CpG motifs can minimize LPS-induced inflammation in the lower respiratory tract through an IL-12 dependent pathway. Journal of Immunology 1999;163:224-231. |
R826711C001 (2000) R826711C002 (2000) |
not available |
|
|
Schwartz DA. Etiology and pathogenesis of airway disease in children and adults from rural communities. Environmental Health Perspectives, 1999; 107 (Suppl 3):393-401. |
R826711C001 (2000) R826711C002 (2000) |
not available |
|
|
Wohlford-Lenane CL, Deetz DC, Schwartz DA. Cytokine gene expression following inhalation of corn dust. American Journal of Physiology: Lung Cell Molecular Biology 1999;276:L736-L743. |
R826711C001 (2000) R826711C002 (2000) |
not available |
asthma, grain dust, airway inflammation, endotoxin. , Scientific Discipline, Health, RFA, Susceptibility/Sensitive Population/Genetic Susceptibility, Biology, Risk Assessments, genetic susceptability, Health Risk Assessment, Children's Health, Atmospheric Sciences, Environmental Chemistry, Allergens/Asthma, environmentally caused disease, allergen, health effects, inhalation, dust , dust mite, rural communities, assessment of exposure, childhood respiratory disease, dust mites, allergic airway, harmful environmental agents, toxics, agricultural community, community-based intervention, sensitive populations, biological response, grain dust, airway disease, children, disease, exposure, children's vulnerablity, asthma, human exposure, Human Health Risk Assessment
Progress and Final Reports:
Original Abstract
Final Report
Main Center Abstract and Reports:
R826711 University of Iowa Children's Environmental Airway Disease Center
Subprojects under this Center:
(EPA does not fund or establish subprojects; EPA awards and manages the overall grant for this center).
R826711C001 Mechanisms that Initiate, Promote, and Resolve Grain Dust/LPS Induced Inflammation
R826711C002 Multi-component Intervention Study of Asthma in Children from Rural Communities
R826711C003 Role of RSV Infection and Endotoxin in Airway Inflammation
R826711C004 A Model to Study the Development of Persistent Environmental Airway Disease