R01HL156277
Project Grant
Overview
Grant Description
Impact of Sleep Duration on Immune Balance in Urban Children with Asthma - Project Summary / Abstract
Urban children with asthma are at high risk for short sleep, due to an environment that jeopardizes sleep and asthma management. Further, this group suffers from altered immune balance, a key biological process contributing to individual differences in asthma morbidity and sleep health.
Allergic asthma is a chronic inflammatory disorder driven primarily by disturbed T helper 1 (Th1)/2 (Th2) cytokine balance marked by Th2 cytokine (IL-4, IL-5, and/or IL-13) predominance. Experimental findings in healthy adults show that shortened sleep increases inflammatory cytokine (e.g., IL-6) and certain Th2 cytokine levels and that recovery sleep following sleep restriction promotes a return to immune balance.
Whether sleep duration plays a key role in immune function and associated asthma activity in urban children with asthma remains a scientific gap. We will use an experimental design that targets sleep duration because (1) the urban environment and asthma symptoms interact to shorten sleep, (2) sleep duration is a modifiable behavior overlooked in clinical care of urban children with asthma, and (3) experimental data are critical to test a causal link for sleep duration as a mechanism underlying immune balance and asthma.
We will enroll urban children (N=204; ages 8-9 years) with persistent allergic asthma and adequate sleep duration (9-11 hours) who will complete a 4-week within-subjects protocol that includes 3 scheduled experimental sleep conditions: (1) 1 week stabilized sleep (individualized; 9-11 hours time in bed), (2) 1 week shortened sleep (1.5-hour decrease in time in bed), and (3) 2 weeks recovery sleep (1.5-hour increase in time in bed).
We will monitor sleep duration (actigraphy) and lung function (home spirometry) daily and assess immune biomarkers weekly and at the midpoint of shortened sleep. To control time-in-study effects, 1/3 of our sample will receive only the stabilized sleep schedule across the 4-week protocol.
In this project, we will study only urban children with allergic asthma who obtain sufficient sleep (9-11 hours, within national guidelines). Our shortened sleep protocol will model the sleep loss that urban children with asthma can experience due to asthma and/or urban context. Additionally, our recovery sleep protocol simulates a sleep optimization intervention following shortened sleep in a well-controlled approach.
The first aim of the study is to examine the effects of shortened sleep on immune balance [e.g., Th1 (interferon-IFN)/Th2 (interleukin-IL-4, IL-5, IL-13)R and plasma IL-6 levels]. The second aim involves determining the effects of recovery sleep on immune balance. The third aim involves examining the extent to which changes in immune balance are associated with changes in asthma-related lung function (changes in FEV1) under conditions of shortened and recovery sleep.
Results from this study ultimately will support the development of feasible, ecologically valid, and clinically meaningful interventions to optimize sleep duration, immune balance, and asthma in this at-risk group.
Urban children with asthma are at high risk for short sleep, due to an environment that jeopardizes sleep and asthma management. Further, this group suffers from altered immune balance, a key biological process contributing to individual differences in asthma morbidity and sleep health.
Allergic asthma is a chronic inflammatory disorder driven primarily by disturbed T helper 1 (Th1)/2 (Th2) cytokine balance marked by Th2 cytokine (IL-4, IL-5, and/or IL-13) predominance. Experimental findings in healthy adults show that shortened sleep increases inflammatory cytokine (e.g., IL-6) and certain Th2 cytokine levels and that recovery sleep following sleep restriction promotes a return to immune balance.
Whether sleep duration plays a key role in immune function and associated asthma activity in urban children with asthma remains a scientific gap. We will use an experimental design that targets sleep duration because (1) the urban environment and asthma symptoms interact to shorten sleep, (2) sleep duration is a modifiable behavior overlooked in clinical care of urban children with asthma, and (3) experimental data are critical to test a causal link for sleep duration as a mechanism underlying immune balance and asthma.
We will enroll urban children (N=204; ages 8-9 years) with persistent allergic asthma and adequate sleep duration (9-11 hours) who will complete a 4-week within-subjects protocol that includes 3 scheduled experimental sleep conditions: (1) 1 week stabilized sleep (individualized; 9-11 hours time in bed), (2) 1 week shortened sleep (1.5-hour decrease in time in bed), and (3) 2 weeks recovery sleep (1.5-hour increase in time in bed).
We will monitor sleep duration (actigraphy) and lung function (home spirometry) daily and assess immune biomarkers weekly and at the midpoint of shortened sleep. To control time-in-study effects, 1/3 of our sample will receive only the stabilized sleep schedule across the 4-week protocol.
In this project, we will study only urban children with allergic asthma who obtain sufficient sleep (9-11 hours, within national guidelines). Our shortened sleep protocol will model the sleep loss that urban children with asthma can experience due to asthma and/or urban context. Additionally, our recovery sleep protocol simulates a sleep optimization intervention following shortened sleep in a well-controlled approach.
The first aim of the study is to examine the effects of shortened sleep on immune balance [e.g., Th1 (interferon-IFN)/Th2 (interleukin-IL-4, IL-5, IL-13)R and plasma IL-6 levels]. The second aim involves determining the effects of recovery sleep on immune balance. The third aim involves examining the extent to which changes in immune balance are associated with changes in asthma-related lung function (changes in FEV1) under conditions of shortened and recovery sleep.
Results from this study ultimately will support the development of feasible, ecologically valid, and clinically meaningful interventions to optimize sleep duration, immune balance, and asthma in this at-risk group.
Awardee
Funding Goals
NOT APPLICABLE
Grant Program (CFDA)
Awarding / Funding Agency
Place of Performance
Providence,
Rhode Island
029034923
United States
Geographic Scope
Single Zip Code
Related Opportunity
Analysis Notes
Amendment Since initial award the total obligations have increased 342% from $763,087 to $3,376,297.
Rhode Island Hospital was awarded
Optimizing Sleep Duration Immune Balance in Urban Children with Asthma
Project Grant R01HL156277
worth $3,376,297
from National Heart Lung and Blood Institute in August 2021 with work to be completed primarily in Providence Rhode Island United States.
The grant
has a duration of 5 years and
was awarded through assistance program 93.837 Cardiovascular Diseases Research.
The Project Grant was awarded through grant opportunity Research Project Grant (Parent R01 Clinical Trial Required).
Status
(Ongoing)
Last Modified 9/5/24
Period of Performance
8/15/21
Start Date
7/31/26
End Date
Funding Split
$3.4M
Federal Obligation
$0.0
Non-Federal Obligation
$3.4M
Total Obligated
Activity Timeline
Subgrant Awards
Disclosed subgrants for R01HL156277
Transaction History
Modifications to R01HL156277
Additional Detail
Award ID FAIN
R01HL156277
SAI Number
R01HL156277-1535859761
Award ID URI
SAI UNAVAILABLE
Awardee Classifications
Nonprofit Without 501(c)(3) IRS Status (Other Than An Institution Of Higher Education)
Awarding Office
75NH00 NIH NATIONAL HEART, LUNG, AND BLOOD INSTITUTE
Funding Office
75NH00 NIH NATIONAL HEART, LUNG, AND BLOOD INSTITUTE
Awardee UEI
N876TLXYGCG4
Awardee CAGE
1HTV4
Performance District
RI-02
Senators
Sheldon Whitehouse
John Reed
John Reed
Budget Funding
Federal Account | Budget Subfunction | Object Class | Total | Percentage |
---|---|---|---|---|
National Heart, Lung, and Blood Institute, National Institutes of Health, Health and Human Services (075-0872) | Health research and training | Grants, subsidies, and contributions (41.0) | $1,681,938 | 100% |
Modified: 9/5/24