ArticleBrain, behavior, and immunity2025
Fueling the fire in the lung-brain axis: The salience network connects allergen-provoked TH17 responses to psychological stress in asthma.
Article in Brain, behavior, and immunity, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 2 of them syntheses that pooled it.
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Who cites it
6 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Violence-Related Distress, Nasal Epithelial Gene Expression, and T17-High Asthma in Youth.Pediatric pulmonology · 2026Pooled it
- A molecular systems architecture of asthma.Frontiers in immunology · 2026Pooled it
- Neural mechanisms of mindfulness-based stress reduction in asthma.Scientific reports · 2026Trial
- Unknotting the nexus of asthma and neuroinflammation: from brain network alterations to therapeutic implications.Journal of neuroinflammation · 2026Review
- Glycolytic reprogramming and cell-specific lactylation in asthma: an evidence-graded framework for testable metabolic-epigenetic profiles.Frontiers in immunology · 2026Review
- Mesenchymal stem cell therapy for breast cancer-related secondary lymphedema (Review).Molecular and clinical oncology · 2025Review
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Authors and funding
8 authors.
Funding
Abstract
backgroundAsthma, a highly prevalent chronic inflammatory disease of the airways, results in an average of 10 deaths per day in the U.S., and psychological stress hinders its effective management. Threat-sensitive neurocircuitry, active during psychological stress, may intensify airway inflammatory responses and contribute to poor clinical outcomes. However, the neural mechanisms and descending pathways connecting acute stress and inflammatory responses to allergen exposure remain poorly understood. We hypothesized that stress-induced engagement of the salience network would prime Th17 immune pathways and potentiate airway inflammation.
methodsWe measured brain glucose metabolism during the Trier Social Stress Test (TSST) and a non-stressful control task using [
resultsAs expected, the WL-AG increased all inflammatory biomarkers. Acute stress significantly increased salivary cortisol (t(27.3) = -27.3, p < 0.01), but did not significantly affect airway inflammation overall. Instead, more robust cortisol responses to stress predicted increased glucose metabolism in the amygdala, insula, and dorsal anterior cingulate cortex, key nodes in the salience network, as well as increased IL-23A mRNA expression (t(22.1) = 2.38, p = 0.026) and FeNO (t(21.5) = 2.17, p = 0.041). Moreover, differential increases in amygdala and dACC glucose metabolism predicted differential increases IL-23A mRNA expression following WL-AG. In addition, compared to low chronic stress, high chronic stress was associated with enhanced IL-17A mRNA expression in response to acute stress and WL-AG.
conclusionsIndividual differences in salience network and cortisol responses to acute stress predict enhanced allergen challenge-provoked Th17-related responses, advancing our understanding of the efferent arm of the lung-brain axis in asthma. This work underscores the importance of translational research for the development of novel interventions that target stress-sensitive brain and immune pathways.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.