ArticleCritical care (London, England)2018
Focal ischemic stroke leads to lung injury and reduces alveolar macrophage phagocytic capability in rats.
Article in Critical care (London, England), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 1 of them a synthesis that pooled it.
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Who cites it
59 citing papers in PubMed, 1 synthesis or guideline pooled it, 82 citations in OpenAlex.
- Immunomodulation for stroke-associated pneumonia: a systematic review of mechanistic insight and emerging therapeutic strategies in animal models.Frontiers in immunology · 2026Pooled it
- Advances in stroke-associated pneumonia in the era of revascularization therapy.Chinese medical journal · 2026Review
- Development and external validation of a risk stratification model for stroke-associated pneumonia.iScience · 2026Article
- The active role of pulmonary immunity in ischaemic stroke.Journal of neuroinflammation · 2026Review
- Article
- Neuroprotective Effects of Phenothiazines on Acute Ischemic Stroke.CNS neuroscience & therapeutics · 2026Review
- PKM2 from hyperactive neuron aggravate lung injury post-stroke by promoting FOXO3A/TXNIP mitochondria translocation in mice.Redox biology · 2026Article
- Pulmonary edema following subarachnoid hemorrhage is associated with impairment of pulmonary vascular endothelial glycocalyx.Biochemistry and biophysics reports · 2026Article
- Baicalin-geniposide attenuates pulmonary inflammation and vascular injury via HMGB1 blockade: insights from a cerebral ischemia-reperfusion model and implications for pulmonary hypertension.Frontiers in pharmacology · 2026Article
- Migrasomes in Ischemic Stroke: Molecular Landscape and Pathophysiological Impact.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Formononetin Protects Against Cerebral Ischemia-Reperfusion-Induced Lung Injury: Insights from Animal and Cell Models.Journal of inflammation research · 2026Article
- Gut dysbiosis, metabolic signals, and pulmonary immune reprogramming: decoding the gut microbiota -immune axis in stroke-associated pneumonia.Frontiers in immunology · 2026Review
- Prediction for Respiratory Failure in Ischemic Stroke Patients Admitted to ICU: A Retrospective Analysis Based on MIMIC-IV Database.Brain and behavior · 2025Article
- Bone marrow-derived emergency monopoiesis drives brain-lung axis injury after traumatic brain injury via IL-1.Journal of neuroinflammation · 2025Article
- The non-invasive transcranial Doppler for hemodynamic monitoring.Physiological research · 2025Article
- Effects of different sodium concentrations in fluids on brain, lung, and kidney in experimental ischemic stroke.Scientific reports · 2025Article
- Gut microbiota dysbiosis drives stroke-associated pneumonia: mechanisms and targeted therapeutic strategies.Frontiers in neuroscience · 2025Review
- Review
- Pinocembrin activation of DPP9 inhibits NLRP1 inflammasome activation to alleviate cerebral ischemia/reperfusion-induced lung and intestinal injury.Immunologic research · 2024Article
- Modeling of the brain-lung axis using organoids in traumatic brain injury: an updated review.Cell & bioscience · 2024Review
Corrections and comments
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Authors and funding
18 authors at 6 institutions in 5 countries.
Funding
Abstract
backgroundIschemic stroke causes brain inflammation, which we postulate may result in lung damage. Several studies have focused on stroke-induced immunosuppression and lung infection; however, the possibility that strokes may trigger lung inflammation has been overlooked. We hypothesized that even focal ischemic stroke might induce acute systemic and pulmonary inflammation, thus altering respiratory parameters, lung tissue integrity, and alveolar macrophage behavior.
methodsForty-eight Wistar rats were randomly assigned to ischemic stroke (Stroke) or sham surgery (Sham). Lung function, histology, and inflammation in the lung, brain, bronchoalveolar lavage fluid (BALF), and circulating plasma were evaluated at 24 h. In vitro, alveolar macrophages from naïve rats (unstimulated) were exposed to serum or BALF from Sham or Stroke animals to elucidate possible mechanisms underlying alterations in alveolar macrophage phagocytic capability. Alveolar macrophages and epithelial and endothelial cells of Sham and Stroke animals were also isolated for evaluation of mRNA expression of interleukin (IL)-6 and tumor necrosis factor (TNF)-α.
resultsTwenty-four hours following ischemic stroke, the tidal volume, expiratory time, and mean inspiratory flow were increased. Compared to Sham animals, the respiratory rate and duty cycle during spontaneous breathing were reduced, but this did not affect lung mechanics during mechanical ventilation. Lungs from Stroke animals showed clear evidence of increased diffuse alveolar damage, pulmonary edema, and inflammation markers. This was associated with an increase in ultrastructural damage, as evidenced by injury to type 2 pneumocytes and endothelial cells, cellular infiltration, and enlarged basement membrane thickness. Protein levels of proinflammatory mediators were documented in the lung, brain, and plasma (TNF-α and IL-6) and in BALF (TNF-α). The phagocytic ability of macrophages was significantly reduced. Unstimulated macrophages isolated from naïve rats only upregulated expression of TNF-α and IL-6 following exposure to serum from Stroke rats. Exposure to BALF from Stroke or Sham animals did not change alveolar macrophage behavior, or gene expression of TNF-α and IL-6. IL-6 expression was increased in macrophages and endothelial cells from Stroke animals.
conclusionsIn rats, focal ischemic stroke is associated with brain-lung crosstalk, leading to increased pulmonary damage and inflammation, as well as reduced alveolar macrophage phagocytic capability, which seems to be promoted by systemic inflammation.
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Registered trials
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.