Are there neurophenotypes for asthma? Functional brain imaging of the interaction between emotion and inflammation in asthma.

Are there neurophenotypes for asthma? Functional brain imaging of the interaction between emotion and inflammation in asthma.
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DOI:
10.1371/journal.pone.0040921
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发表时间:
2012
期刊:
影响因子:
3.7
通讯作者:
Davidson RJ
Davidson RJ
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Rosenkranz MA;Busse WW;Sheridan JF;Crisafi GM;Davidson RJ

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哮喘是一种慢性炎症性疾病,值得注意的是其易受压力和情绪诱导的症状加剧。心理压力、情绪和焦虑障碍似乎增加了哮喘症状的表达,这一事实表明大脑和肺之间的神经信号至少部分调节了炎症反应和肺功能。然而,涉及调节哮喘症状的神经通路的确切性质尚不清楚。此外,神经信号的变化在多大程度上预测疾病表达的不同表型尚未研究。我们使用功能性磁共振成像来测量神经信号对哮喘特异性情绪线索的反应,在过敏原暴露后,在对过敏原挑战有双重反应的哮喘患者(显著炎症)中,只有立即反应的哮喘患者(最小炎症)和健康对照组。在哮喘患者双重反应的晚期阶段,与一般的负性提示相比,哮喘相关的提示可以不同程度地激活前岛叶皮层。此外,这种差异激活的程度预测气道炎症的变化。这些发现表明,哮喘的神经表型可以通过已知参与处理情绪信息的脑回路的神经反应来识别。那些在前额叶有更大激活的人,在对哮喘相关的心理刺激的反应中,在肺部表现出更大的炎症信号,疾病的严重程度增加,可能反映了哮喘患者中最容易发展为精神病理学的一个子集。这种方法为哮喘的潜在治疗干预提供了一个全新的靶点。
Asthma is a chronic inflammatory disease noteworthy for its vulnerability to stress and emotion-induced symptom intensification. The fact that psychological stress and mood and anxiety disorders appear to increase expression of asthma symptoms suggests that neural signaling between the brain and lung at least partially modulates the inflammatory response and lung function. However, the precise nature of the neural pathways implicated in modulating asthma symptoms is unknown. Moreover, the extent to which variations in neural signaling predict different phenotypes of disease expression has not been studied. We used functional magnetic resonance imaging to measure neural signals in response to asthma-specific emotional cues, following allergen exposure, in asthmatics with a dual response to allergen challenge (significant inflammation), asthmatics with only an immediate response (minimal inflammation), and healthy controls. The anterior insular cortex was differentially activated by asthma-relevant cues, compared to general negative cues, during the development of the late phase of the dual response in asthmatics. Moreover, the degree of this differential activation predicted changes in airway inflammation. These findings indicate that neurophenotypes for asthma may be identifiable by neural reactivity of brain circuits known to be involved in processing emotional information. Those with greater activation in the anterior insula, in response to asthma-relevant psychological stimuli, exhibit greater inflammatory signals in the lung and increased severity of disease and may reflect a subset of asthmatics most vulnerable to the development of psychopathology. This approach offers an entirely new target for potential therapeutic intervention in asthma.
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