Center for Healthy Minds, University of Wisconsin-Madison, 625 W. Washington Ave, Madison, WI 53703, USA.
Department of Radiology, University of Wisconsin School of Medicine and Public Health, Madison, 600 Highland Ave, Madison, WI 53792, USA.
Brain Behav Immun. 2024 Nov;122:9-17. doi: 10.1016/j.bbi.2024.07.042. Epub 2024 Aug 2.
Inflammation is an established contributor to the pathophysiology of depression and the prevalence of depression in those with chronic inflammatory disease is two- to four-fold higher than the general population. Yet little is known about the neurobiological changes that confer depression or resilience to depression, that occur when episodes of heightened inflammation are frequent or span many years.
We used an innovative combination of longitudinal resting state functional magnetic resonance imaging coupled to segmental bronchial provocation with allergen (SBP-Ag) to assess changes in resting state functional connectivity (rsFC) of the salience network (SN) caused by an acute inflammatory exacerbation in twenty-six adults (15 female) with asthma and varying levels of depressive symptoms. Eosinophils measured in bronchoalveolar lavage fluid and blood provided an index of allergic inflammation and the Beck Depression Inventory provided an index of depressive symptoms.
We found that in those with the highest symptoms of depression at baseline, SN rsFC declined most from pre- to post-SBP-Ag in the context of a robust eosinophilic response to challenge, but in those with low depressive symptoms SN rsFC was maintained or increased, even in those with the most pronounced SBP-Ag response.
Thus, the maintenance of SN rsFC during inflammation may be a biomarker of resilience to depression, perhaps via more effective orchestration of large-scale brain network dynamics by the SN. These findings advance our understanding of the functional role of the SN during inflammation and inform treatment recommendations for those with comorbid inflammatory disease and depression.
炎症是抑郁症病理生理学的既定诱因,患有慢性炎症性疾病的抑郁症患病率比普通人群高 2 至 4 倍。然而,人们对在炎症发作频繁或持续多年时导致抑郁症或对抑郁症具有抵抗力的神经生物学变化知之甚少。
我们使用了一种创新的组合方法,即结合纵向静息态功能磁共振成像和支气管分段激发试验(SBP-Ag)来评估 26 名(15 名女性)哮喘患者和不同程度抑郁症状的静息状态功能连接(rsFC)的变化。支气管肺泡灌洗液和血液中的嗜酸性粒细胞提供了过敏炎症的指标,贝克抑郁量表提供了抑郁症状的指标。
我们发现,在基线时抑郁症状最严重的患者中,在挑战时嗜酸性粒细胞反应强烈的情况下,SN rsFC 从 SBP-Ag 前到后下降最多,但在抑郁症状较轻的患者中,SN rsFC 保持或增加,即使在 SBP-Ag 反应最明显的患者中也是如此。
因此,在炎症期间 SN rsFC 的维持可能是对抑郁症具有抵抗力的生物标志物,这可能是通过 SN 更有效地协调大脑网络的大规模动态。这些发现推进了我们对炎症期间 SN 功能作用的理解,并为患有炎症性疾病和抑郁症的患者提供了治疗建议。