Biomarkers in Acute Lung Injury: Insights into the Pathogenesis of Acute Lung Injury

Cross, L.J.M.; Matthay, Michael A.

doi:10.1016/j.ccc.2010.12.005

Cited by 206 publications

(192 citation statements)

References 158 publications

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“…The migration and accumulation of inflammatory factors and apoptotic factors can produce large amount of oxygen free radicals and protease, resulting in pulmonary capillary endothelial cell and alveolar epithelial cell injuries 11 and ultimately leads to cell apoptosis, causing ALI. Previous studies showed that many pro-inflammatory cytokines such as IL-8 and IL-6 contributed to the induction of ALI 12 . In the present study, we provided additional evidences that MIRI, on one hand, increased cell apoptosis in the lung; on the other hand, increased pro-inflammatory cytokines release (IL-6 and IL-8) and reduced anti-inflammatory cytokine (IL-10) release, resulting in enhanced inflammation in the lung, and caused ALI.…”

Section: ■ Discussionmentioning

confidence: 99%

Myocardial ischemic post-conditioning protects the lung against myocardial ischemia/reperfusion-induced damage by activating GSK-3β

et al. 2017

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Myocardial ischemic post-conditioning protects the lung against myocardial ischemia/reperfusion-induced damage by activating GSK-3β 1 Abstract Purpose: To investigate whether modulating GSK-3β could attenuate myocardial ischemia reperfusion injury (MIRI) induced acute lung injury (ALI) and analyze the underlying mechanism. Methods: Male SD rats were subjected to MIRI with or without myocardial ischemic postconditioning in the presence or absence of GSK-3β inhibitor. GSK-3β inhibitor was injected peritoneally 10min before MIRI. Lung W/D weight ratio, MPO, PMNs, histopathological changes, TUNEL, Bax, Bcl-2, IL-6, IL-8, IL-10, GSK-3β, and caspase-3 were evaluated in the lung tissues of all rats. Results: After MIRI, lung injury was significantly increased manifested as significant morphological changes and increased leukocytes in the interstitial capillaries, Lung W/D ratio, MPO, and PMN in BALF, which was associated with enhanced inflammation evidenced by increased expressions of IL-6, IL-8 and reduced expression of IL-10. MIRI significantly increased cell apoptosis in the lung as increased levels of apoptotosis, Bax, cleaved caspase-3, and reduced expression of Bcl-2 was observed, which was concomitant with reduced p-GSK-3β. All these changes were reversed/prevented by ischemic post-conditioning, while these beneficial effects of ischemic post-conditioning were abolished by GSK-3β inhibition. Conclusion: Myocardial ischemia reperfusion injury induces acute lung injury by induction of inflammation and cell apoptosis. Ischemic post-conditioning protects the lung from ALI following MIRI by increasing p-GSK-3β.

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Section: ■ Discussionmentioning

confidence: 99%

Myocardial ischemic post-conditioning protects the lung against myocardial ischemia/reperfusion-induced damage by activating GSK-3β

et al. 2017

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“…30,31 In the pathogenesis of ALI, extensive cytokines and ROS were released. 32 Inflammation initiated by oxidative stress can be regulated by the RvD1. 9 One of our previous studies on 15-epi-16-parafluorophenoxy lipoxin A4 (ATL), an analogue of RvD1, have found that ATL not only increased HO-1 expression but also markedly diminished all markers of lung injury.…”

Section: Discussionmentioning

confidence: 99%

Resolvin D1 reduces deterioration of tight junction proteins by upregulating HO-1 in LPS-induced mice

Xie

Wang

et al. 2013

Laboratory Investigation

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Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) is characterized by increased pulmonary permeability with high mortality. Resolvin D1 (RvD1), which has potent anti-inflammatory and pro-resolving activity, can attenuate pulmonary edema in the animal model of ALI. However, the mechanism underlying the protection of RvD1 on pulmonary edema is still unknown. Here we explore the effects and mechanism of RvD1 on the disruption of tight junction protein that results in the permeability edema in a model of lipopolysaccharide (LPS)-induced ALI. The severity of pulmonary edema was assessed by wet-to-dry rate and Evans blue infiltration; expressions of tight junction (TJ) proteins occludin and zona occludin-1 (ZO-1) were examined by immunofluorescence staining and western blot; mRNA in lung tissue was studied by real time-PCR; the TUNEL kit was performed for the detection of apoptosis of pulmonary barrier. Twenty-four hours after LPS inhalation by mice, wet-to-dry rate and Evans blue infiltration indicated that pretreatment with RvD1 relieved the pulmonary edema and pulmonary capillary permeability. Moreover, RvD1 attenuated the LPS-induced deterioration of TJ protein ZO-1 and occludin significantly. And we found that RvD1 increased heme oxygenase-1 (HO-1) expression contributed to the protection on the deterioration of TJs. In addition, we found that RvD1 could reduce pulmonary cellular apoptosis in LPS-induced mice. In conclusion, RvD1 possesses the ability that relieves the pulmonary edema and restores pulmonary capillary permeability and reduces disruption of TJs in LPS-induced ALI of mice, at least in part, by upregulating HO-1 expression.

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“…Donnelly et al (41) noted that increased BAL IL-8 secretion and increased alveolar macrophage IL-8 expression was associated with progression to ARDS among at-risk patients with significant systemic inflammation. Additionally, increased BAL IL-8 was associated with increased mortality in patients with established ARDS (31,116,121).…”

Section: Macrophage Function During Human Ardsmentioning

confidence: 99%

Diverse macrophage populations mediate acute lung inflammation and resolution

Aggarwal

King

D’Alessio

2014

American Journal of Physiology-Lung Cellular and Molecular Phys

480

408

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Biomarkers in Acute Lung Injury: Insights into the Pathogenesis of Acute Lung Injury

Cited by 206 publications

References 158 publications

Myocardial ischemic post-conditioning protects the lung against myocardial ischemia/reperfusion-induced damage by activating GSK-3β

Myocardial ischemic post-conditioning protects the lung against myocardial ischemia/reperfusion-induced damage by activating GSK-3β

Resolvin D1 reduces deterioration of tight junction proteins by upregulating HO-1 in LPS-induced mice

Diverse macrophage populations mediate acute lung inflammation and resolution

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