WHAT REALLY CAUSES EXERCISE-INDUCED ASTHMA IN CHILDREN?
WHAT REALLY CAUSES EXERCISE-INDUCED ASTHMA IN CHILDREN?
批准号:
8166896
负责人:
DAN M COOPER
金额:
$0.72万
依托单位国家:
美国
项目类别:
财政年份:
2009
资助国家:
美国
项目状态:
已结题
起止时间:
2009-12-01 至 2010-06-30
关键词:
AddressAdultAsthmaBronchoconstrictionChildChildhood AsthmaComputer Retrieval of Information on Scientific Projects DatabaseExerciseExercise-Induced AsthmaFundingGoalsGrantICAM1 geneInflammatory ResponseInstitutionIntercellular adhesion molecule 1Interleukin-1Interleukin-1 betaInterleukin-6LaboratoriesLungMediator of activation proteinPatientsPeripheral Blood Mononuclear CellPlayRecording of previous eventsResearchResearch PersonnelResourcesRoleSourceTestingTumor Necrosis Factor-alphaUnited States National Institutes of HealthWheezingbasecytokineresponse
中文摘要
这个子项目是许多研究子项目中的一个
由NIH/NCRR资助的中心赠款提供的资源。子项目和
研究者(PI)可能从另一个NIH来源获得了主要资金,
因此可以在其他CRISP条目中表示。所列机构为
研究中心,而研究中心不一定是研究者所在的机构。
本研究的目的是开始验证一个假设,即哮喘儿童对运动的异常强烈的全身性而不是肺部细胞因子和细胞间粘附分子-1(ICAM-1,也称为CD 54)反应可能在运动诱导的支气管收缩(EIB)现象中发挥作用。 这个新的假设是基于丹库珀博士实验室最近的观察。 现在很清楚,相对短暂的剧烈运动刺激促炎细胞因子(即,白细胞介素-1 β,白细胞介素-6和肿瘤坏死因子-α)和ICAM-1在无哮喘病史的健康儿童外周血单核细胞的表达。 这是一个有趣的发现,因为促炎介质如IL-1和ICAM-I可能在支气管哮喘中起作用,并且在绝大多数儿童哮喘患者中发现了运动诱导的喘息。 因此,我们有理由假设,哮喘儿童对运动的全身炎症反应可能异常强烈,并有助于EIB的机制。 这一假设尚未在成人或儿童中得到解决。
英文摘要
This subproject is one of many research subprojects utilizing the
resources provided by a Center grant funded by NIH/NCRR. The subproject and
investigator (PI) may have received primary funding from another NIH source,
and thus could be represented in other CRISP entries. The institution listed is
for the Center, which is not necessarily the institution for the investigator.
The goal of this research is to begin to test the hypothesis that an abnormally robust systemic, rather than pulmonary, cytokine and intercellular adhesion molecule-1 (ICAM-I, known also as CD54) response to exercise in asthmatic children may play a role in the phenomenon of exercise induced bronchoconstriction (EIB). This new hypothesis is based on observations recently made in the laboratory of Dr. Dan Cooper. It is now clear that relatively brief episodes of intense exercise stimulate proinflammatory cytokines (namely, interleukin-1 beta, interleukin-6, and tumor necrosis factor-alpha) and ICAM-I expression on peripheral blood mononuclear cells in healthy children with no history of asthma. This is an intriguing finding since proinflammatory mediators like IL-1 and ICAM-I may play a role in bronchial asthma, and exercise-induced wheezing is found in the vast majority of patients with childhood asthma. Thus, it is reasonable to hypothesize that these systemic inflammatory responses to exercise may be abnormally robust in asthmatic children and contribute to the mechanisms responsible for EIB. This hypothesis has not yet been addressed in either adults or children.
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