{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,21]],"date-time":"2026-10-21T19:29:21Z","timestamp":1792610961639,"version":"4.5.0"},"reference-count":246,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,7,3]],"date-time":"2026-07-03T00:00:00Z","timestamp":1783036800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Neurosci."],"abstract":"<jats:p>\n                    Neurogenic pulmonary edema (NPE) is a life-threatening complication of acute central nervous system (CNS) injury, characterized by the rapid onset of hypoxemia and pulmonary fluid accumulation in the absence of underlying cardiopulmonary disease. In recent years, emerging integrative frameworks such as the \u201cneuroimmunoaxis\u201d and \u201cbrain-lung axis\u201d have provided new perspectives on how CNS injury leads to systemic immune dysregulation and pulmonary dysfunction. However, critical questions remain regarding the interplay between excessive sympathetic activation, immune homeostasis disruption, and lung tissue injury. This narrative review proposes a neurotransmitter-immune-inflammatory model that integrates mechanical, adrenergic, and inflammatory pathways across the spatiotemporal evolution of NPE. We identify four progressive stages involving sympathetic storm initiation due to central autonomic network disinhibition, pulmonary vascular barrier disruption through Piezo channel activation and angiotensin II-norepinephrine synergy, inflammatory amplification from loss of the cholinergic anti-inflammatory reflex, and systemic progression involving gut-lung axis dysregulation. The model generates three testable predictions. Lesions disrupting the nucleus tractus solitarius-ventromedial hypothalamus-intermediolateral column projection should produce more severe NPE. And selective activation of TRPA1\n                    <jats:sup>+<\/jats:sup>\n                    dorsal root ganglion neurons should attenuate sympathetic outflow and pulmonary edema. Enhancing \u03b17 nicotinic acetylcholine receptor signaling should mitigate systemic inflammation. These predictions offer experimental avenues for validating the hijacking hypothesis. Translational implications include stage-specific interventions, early sympathetic blockade, mid-phase anti-inflammatory and neuro-modulatory strategies, and late-stage lung-protective ventilation. This study aims to offer a comprehensive analysis of NPE by exploring its pathological mechanisms\u2014from central sympathetic signaling to peripheral lung damage. Emphasis is placed on examining the interactions between neural signals, neurotransmitters, and immune responses to uncover the spatiotemporal dynamics of NPE. By identifying potential pathways for early diagnosis and targeted therapies, the research seeks to improve disease management and contribute to better clinical outcomes for affected patients.\n                  <\/jats:p>","DOI":"10.3389\/fnins.2026.1821390","type":"journal-article","created":{"date-parts":[[2026,7,3]],"date-time":"2026-07-03T05:40:05Z","timestamp":1783057205000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":1,"title":["From sympathetic storm to systemic inflammation: spatiotemporal dynamics of the brain-lung axis in neurogenic pulmonary edema"],"prefix":"10.3389","volume":"20","author":[{"given":"Mingxin","family":"Zhang","sequence":"first","affiliation":[{"name":"Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University","place":["Beijing, China"]},{"name":"Chinese Institutes for Medical Research","place":["Beijing, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Peng","family":"Zhang","sequence":"additional","affiliation":[{"name":"Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University","place":["Beijing, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2026,7,3]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"351","DOI":"10.1186\/s12888-022-04007-w","article-title":"Angiotensin I converting enzyme gene polymorphisms and risk of psychiatric disorders.","volume":"22","author":"Akbari","year":"2022","journal-title":"BMC Psychiatry"},{"key":"B2","volume-title":"Neurogenic Pulmonary Edema.","author":"Al-Dhahir","year":"2025"},{"key":"B3","doi-asserted-by":"publisher","first-page":"5386","DOI":"10.1038\/s41467-020-19167-0","article-title":"Over-activation of primate subgenual cingulate cortex enhances the cardiovascular, behavioral and neural responses to threat.","volume":"11","author":"Alexander","year":"2020","journal-title":"Nat. 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