Blood Glutamate Levels Are Closely Related to Acute Lung Injury and Prognosis after Stroke

Bai, Wei; Li, Wei; Ning, Yuping; Li, Ping; Zhao, Yan; Yang, Nan; Jiang, Yulin; Liang, Zhongxing; Jiang, Dongpo; Wang, Ying; Zhang, Meng; Zhou, Yuanguo

doi:10.3389/fneur.2017.00755

Cited by 19 publications

(18 citation statements)

References 43 publications

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“…In parallel, the phagocytic capability of alveolar macrophages was decreased. Remarkably, all of these changes occurred within 24 h after the induction of cerebral ischemia, which is in agreement with the rapid onset of ALI in stroke patients [ 7 ]. In-vitro experiments revealed that the phagocytic capability of alveolar macrophages was reduced and the expression of TNF-α and IL-6 was increased in alveolar macrophages isolated from naïve rats only after exposure to serum from rats that had experienced ischemic stroke.…”

Section: Discussionsupporting

confidence: 74%

“…Notably, the lungs are particularly vulnerable in the event of severe brain damage, including ischemic and hemorrhagic strokes [ 5 – 8 ]. Bai et al [ 7 ] reported that 15.6% of stroke patients developed acute lung injury within 36 h of hospital admission, and 7.8% of patients had pneumonia or bronchitis during hospitalization. Studies in experimental models of stroke have focused on stroke-induced immunosuppression and lung infection [ 9 – 13 ], whereas lung injury and inflammation, and their effects on the phagocytic capability of alveolar macrophages, have been overlooked.…”

Section: Introductionmentioning

confidence: 99%

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Focal ischemic stroke leads to lung injury and reduces alveolar macrophage phagocytic capability in rats

Samary¹,

Ramos²,

Maia³

et al. 2018

Crit Care

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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.Electronic supplementary materialThe online version of this article (10.1186/s13054-018-2164-0) contains supplementary material, which is available to authorized users.

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Section: Discussionsupporting

confidence: 74%

Section: Introductionmentioning

confidence: 99%

Focal ischemic stroke leads to lung injury and reduces alveolar macrophage phagocytic capability in rats

Samary¹,

Ramos²,

Maia³

et al. 2018

Crit Care

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“…It has also been shown that experimental stroke in mice induces a peripheral inflammatory response that peaks 4 h after stroke and precedes the peak in brain inflammation 24 h after stroke 21 . A recent study has shown that ALI appears to occur within 24 h of ischemic stroke 22 . These findings suggest that an investigation of lung inflammation and injury induced by stroke would need to draw a focus on the hours shortly after a stroke.…”

Section: Introductionmentioning

confidence: 99%

Ischaemic stroke in mice induces lung inflammation but not acute lung injury

Austin

Miller

et al. 2019

Sci Rep

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Stroke is a major cause of death worldwide and ischemic stroke is the most common subtype accounting for approximately 80% of all cases. Pulmonary complications occur in the first few days to weeks following ischemic stroke and are a major contributor to morbidity and mortality. Acute lung injury (ALI) occurs in up to 30% of patients with subarachnoid haemorrhage but the incidence of ALI after ischemic stroke is unclear. As ischemic stroke is the most common subtype of stroke, it is important to understand the development of ALI following the initial ischemic injury to the brain. Therefore, this study investigated whether focal ischemic stroke causes lung inflammation and ALI in mice. Ischemic stroke caused a significant increase in bronchoalveolar lavage fluid (BALF) macrophages and neutrophils and whole lung tissue proinflammatory IL-1β mRNA expression but this did not translate into histologically evident ALI. Thus, it appears that lung inflammation, but not ALI, occurs after experimental ischemic stroke in mice. This has significant implications for organ donors as the lungs from patient’s dying of ischemic stroke are not severely damaged and could thus be used for transplantation in people awaiting this life-saving therapy.

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“…The lungs are particularly vulnerable in patients with severe brain damage, including ischemic and hemorrhagic strokes (37, 38). It has been shown that ischemic stroke caused excessive leukocyte infiltration into lung and reduced alveolar macrophage phagocytic capability, which contributes importantly to poststroke lung injury (39).…”

Section: Discussionmentioning

confidence: 99%

Inhibition of CD147 Attenuates Stroke-Associated Pneumonia Through Modulating Lung Immune Response in Mice

et al. 2019

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Background and Purpose: Acute ischemic stroke triggers a profound systemic and local immunodysfunction that increased the susceptibility to infections, especially stroke-associated pneumonia (SAP). Our previous study has shown that inhibition of CD147 ameliorates acute ischemic stroke, however, the role of CD147 in post-stroke lung infection has not been investigated. Methods: C57BL/6 mice were subjected to transient (60 min) middle cerebral artery occlusion, and treated with anti-CD147 antibody (αCD147). Lung histological changes, vascular permeability, and pulmonary edema were determined. Bacterial burden in the lung tissue and Broncho alveolar lavage fluid (BALF) were measured. Lung leukocyte infiltration, circulating platelet-leukocyte aggregates, cell type-specific IL-17A, and IFN-γ expression in the lung were detected by flow cytometry. Results: CD147 expression was markedly upregulated in the lung after stroke. αCD147 treatment significantly decreased the stroke-associated lung histological damages, bacterial load, vascular permeability and pulmonary edema. The protective effects by αCD147 treatment were associated with deceased lung inflammatory cell infiltration by reducing IL-17A expression in lung γδ T cells and attenuated bacterial load by enhancing IFN-γ expression in the lung NK1.1 + cells and CD4 + T cells. In addition, CD147 expression was also increased in the circulating platelets and leukocytes. Enhanced platelet-leukocyte aggregates following stroke was inhibited by αCD147 treatment. Conclusions: Inhibition of CD147 ameliorates aberrant lung inflammatory and immune response and reduces bacterial infection after stroke. CD147 might represent a novel and promising therapeutic target for post-stroke lung infection.

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Blood Glutamate Levels Are Closely Related to Acute Lung Injury and Prognosis after Stroke

Cited by 19 publications

References 43 publications

Focal ischemic stroke leads to lung injury and reduces alveolar macrophage phagocytic capability in rats

Focal ischemic stroke leads to lung injury and reduces alveolar macrophage phagocytic capability in rats

Ischaemic stroke in mice induces lung inflammation but not acute lung injury

Inhibition of CD147 Attenuates Stroke-Associated Pneumonia Through Modulating Lung Immune Response in Mice

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