Role of Extracellular Adenosine in Acute Lung Injury

Physiology ◽  
2009 ◽  
Vol 24 (5) ◽  
pp. 298-306 ◽  
Author(s):  
Tobias Eckle ◽  
Michael Koeppen ◽  
Holger K. Eltzschig
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Lung Disease ◽  
Pulmonary Edema ◽  
Lung Inflammation ◽  
Severe Hypoxia ◽  
Extracellular Adenosine ◽  
The Past

Acute lung injury (ALI) is a lung disease characterized by pulmonary edema and severe hypoxia. The past decade hosted a search for endogenous mechanisms controlling lung inflammation and pulmonary edema during ALI. As such, recent evidence indicates extracellular adenosine in orchestrating the resolution of pulmonary edema and inflammation during ALI.

scholarly journals Global Trends in Research of Macrophages Associated With Acute Lung Injury Over Past 10 Years: A Bibliometric Analysis

2021 ◽  
Vol 12 ◽  
Author(s):  
Sheng Wang ◽  
Huanping Zhou ◽  
Li Zheng ◽  
Wanli Zhu ◽  
Lina Zhu ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Bibliometric Analysis ◽  
Scientific Output ◽  
Annual Number ◽  
Global Trends ◽  
Citation Score ◽  
The Past ◽  
The Usa

Acute lung injury (ALI) is an intractable disorder associated with macrophages. This bibliometric analysis was applied to identify the characteristics of global scientific output, the hotspots, and frontiers about macrophages in ALI over the past 10 years. We retrieved publications published from 2011 to 2020 and their recorded information from Science Citation Index Expanded (SCI-expanded) of Web of Science Core Collection (WoSCC). Bibliometrix package was used to analyze bibliometric indicators, and the VOSviewer was used to visualize the trend and hotspots of researches on macrophages in ALI. Altogether, 2,632 original articles were reviewed, and the results showed that the annual number of publications (Np) concerning the role of macrophages in ALI kept increasing over the past 10 years. China produced the most papers, the number of citations (Nc) and H-index of the USA ranked first. Shanghai Jiaotong University and INT IMMUNOPHARMACOL were the most prolific affiliation and journal, respectively. Papers published by Matute-Bello G in 2011 had the highest local citation score (LCS). Recently, the keywords “NLRP3” and “extracellular vesicles” appeared most frequently. Besides, researches on COVID-19–induced ALI related to macrophages seemed to be the hotspot recently. This bibliometric study revealed that publications related to macrophages in ALI tend to increase continuously. China was a big producer and the USA was an influential country in this field. Most studies were mainly centered on basic researches in the past decade, and pathways associated with the regulatory role of macrophages in inhibiting and attenuating ALI have become the focus of attention in more recent studies. What is more, our bibliometric analysis showed that macrophages play an important role in COVID-19–induced ALI and may be a target for the treatment of COVID-19.

scholarly journals Mitochondrial peptides cause proinflammatory responses in the alveolar epithelium via FPR-1, MAPKs, and AKT: a potential mechanism involved in acute lung injury

2018 ◽  
Vol 315 (5) ◽  
pp. L775-L786 ◽  
Author(s):  
Xue Zhang ◽  
Tao Wang ◽  
Zhi-Cheng Yuan ◽  
Lu-Qi Dai ◽  
Ni Zeng ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Lung Inflammation ◽  
Cell Injury ◽  
Specific Inhibitor ◽  
Alveolar Epithelium ◽  
Formyl Peptide Receptor ◽  
Potential Mechanism ◽  
Alveolar Epithelial

Acute lung injury (ALI) is characterized by alveolar epithelial damage and uncontrolled pulmonary inflammation. Mitochondrial damage-associated molecular patterns (DAMPs), including mitochondrial peptides [ N-formyl peptides (NFPs)], are released during cell injury and death and induce inflammation by unclear mechanisms. In this study, we have investigated the role of mitochondrial DAMPs (MTDs), especially NFPs, in alveolar epithelial injury and lung inflammation. In murine models of ALI, high levels of mitochondrial NADH dehydrogenase 1 in bronchoalveolar lavage fluid (BALF) were associated with lung injury scores and increased formyl peptide receptor (FPR)-1 expression in the alveolar epithelium. Cyclosporin H (CsH), a specific inhibitor of FPR1, inhibited lung inflammation in the ALI models. Both MTDs and NFPs upon intratracheal challenge caused accumulation of neutrophils into the alveolar space with elevated BALF levels of mouse chemokine KC, interleukin-1β, and nitric oxide and increased pulmonary FPR-1 levels. CsH significantly attenuated MTDs or NFP-induced inflammatory lung injury and activation of MAPK and AKT pathways. FPR1 expression was present in rat primary alveolar epithelial type II cells (AECIIs) and was increased by MTDs. CsH inhibited MTDs or NFP-induced CINC-1/IL-8 release and phosphorylation of p38, JNK, and AKT in rat AECII and human cell line A549. Inhibitors of MAPKs and AKT also suppressed MTD-induced IL-8 release and NF-κB activation. Collectively, our data indicate an important role of the alveolar epithelium in initiating immune responses to MTDs released during ALI. The potential mechanism may involve increase of IL-8 production in MTD-activated AECII through FPR-1 and its downstream MAPKs, AKT, and NF-κB pathways.

scholarly journals Endocan regulates acute lung inflammation through control of leukocyte diapedesis

2019 ◽  
Vol 127 (3) ◽  
pp. 668-678 ◽  
Author(s):  
Alexandre Gaudet ◽  
Lucie Portier ◽  
Méline Prin ◽  
Marie-Christine Copin ◽  
Anne Tsicopoulos ◽  
...  
Keyword(s):  
Acute Respiratory Distress Syndrome ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Lung Inflammation ◽  
Distress Syndrome ◽  
Human Leukocyte ◽  
Transendothelial Migration ◽  
Acute Lung Inflammation ◽  
Leukocyte Transendothelial Migration

Acute respiratory distress syndrome is a severe form of respiratory failure, occurring in up to 20% of patients admitted to the intensive care unit with sepsis. Dysregulated leukocyte diapedesis is a major contributor to acute respiratory distress syndrome. Endocan is a circulating proteoglycan that binds to the leukocyte integrin leukocyte functional antigen-1 and blocks its interaction with its endothelial ligand, ICAM-1. The objective of this study was to evaluate the role of endocan in the control of acute lung inflammation. In vitro, endocan inhibited human leukocyte transendothelial migration as well as ICAM-1-dependent migration but had a very mild effect on ICAM-1-dependent adhesion. Endocan also acted as an inhibitor of transendothelial migration of mouse leukocytes. The effect of systemic administration of recombinant human endocan was assessed in a model of acute lung inflammation in BALB/c mice. Treatment with endocan 1 h after intratracheal LPS challenge reduced the alveolar inflammatory response, diminished histological features of acute lung injury, and improved respiratory function. These results highlight the anti-inflammatory role of human endocan and its protective effect against acute lung injury. NEW & NOTEWORTHY We show here that endocan inhibits ICAM-1-dependent human leukocyte transendothelial migration and ICAM-1-dependent adhesion. We also found that in BALB/c mice with tracheal LPS-induced acute lung injury treatment with recombinant human endocan reduces lung inflammation, notably through reduction of neutrophilic recruitment, and restores normal lung function. These results confirm the hypothesis that human endocan may have a protective effect against acute lung inflammation.

scholarly journals Surfactant Attenuates Air Embolism-Induced Lung Injury by Suppressing NKCC1 Expression and NF-κB Activation

Inflammation ◽  
2020 ◽  
Author(s):  
Chou-Chin Lan ◽  
Yao-Kuang Wu ◽  
Chung-Kan Peng ◽  
Kun-Lun Huang ◽  
Chin-Pyng Wu
Keyword(s):  
Lung Injury ◽  
Pulmonary Edema ◽  
Inflammatory Cytokines ◽  
Lung Inflammation ◽  
Inflammatory Responses ◽  
Air Embolism ◽  
Lower Surface ◽  
Beneficial Effects ◽  
Pro Inflammatory Cytokines

Abstract Excessive amounts of air can enter the lungs and cause air embolism (AE)-induced acute lung injury (ALI). Pulmonary AE can occur during diving, aviation, and iatrogenic invasive procedures. AE-induced lung injury presents with severe hypoxia, pulmonary hypertension, microvascular hyper-permeability, and severe inflammatory responses. Pulmonary AE-induced ALI is a serious complication resulting in significant morbidity and mortality. Surfactant is abundant in the lungs and its function is to lower surface tension. Earlier studies have explored the beneficial effects of surfactant in ALI; however, none have investigated the role of surfactant in pulmonary AE-induced ALI. Therefore, we conducted this study to determine the effects of surfactant in pulmonary AE-induced ALI. Isolated-perfused rat lungs were used as a model of pulmonary AE. The animals were divided into four groups (n = 6 per group): sham, air embolism (AE), AE + surfactant (0.5 mg/kg), and AE+ surfactant (1 mg/kg). Surfactant pretreatment was administered before the induction of pulmonary AE. Pulmonary AE was induced by the infusion of 0.7 cc air through a pulmonary artery catheter. After induction of air, pulmonary AE was presented with pulmonary edema, pulmonary microvascular hyper-permeability, and lung inflammation with neutrophilic sequestration. Activation of NF-κB was observed, along with increased expression of pro-inflammatory cytokines, and Na-K-Cl cotransporter isoform 1 (NKCC1). Surfactant suppressed the activation of NF-κB and decreased the expression of pro-inflammatory cytokines and NKCC1, thereby attenuating AE-induced lung injury. Therefore, AE-induced ALI presented with pulmonary edema, microvascular hyper-permeability, and lung inflammation. Surfactant suppressed the expressions of NF-κB, pro-inflammatory cytokines, and NKCC1, thereby attenuating AE-induced lung injury.

scholarly journals Macrophage micro-RNA-155 promotes lipopolysaccharide-induced acute lung injury in mice and rats

2016 ◽  
Vol 311 (2) ◽  
pp. L494-L506 ◽  
Author(s):  
Wen Wang ◽  
Zhi Liu ◽  
Jie Su ◽  
Wen-Sheng Chen ◽  
Xiao-Wu Wang ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Alveolar Macrophages ◽  
Lung Inflammation ◽  
Micro Rna ◽  
Pcr Analysis ◽  
Cytokine Signaling ◽  
Wild Type

Micro-RNA (miR)-155 is a novel gene regulator with important roles in inflammation. Herein, our study aimed to explore the role of miR-155 in LPS-induced acute lung injury(ALI). ALI in mice was induced by intratracheally delivered LPS. Loss-of-function experiments performed on miR-155 knockout mice showed that miR-155 gene inactivation protected mice from LPS-induced ALI, as manifested by preserved lung permeability and reduced lung inflammation compared with wild-type controls. Bone marrow transplantation experiments identified leukocytes, but not lung parenchymal-derived miR-155-promoted acute lung inflammation. Real-time PCR analysis showed that the expression of miR-155 in lung tissue was greatly elevated in wild-type mice after LPS stimulation. In situ hybridization showed that miR-155 was mainly expressed in alveolar macrophages. In vitro experiments performed in isolated alveolar macrophages and polarized bone marrow-derived macrophages confirmed that miR-155 expression in macrophages was increased in response to LPS stimulation. Conversely, miR-155 gain-of-function in alveolar macrophages remarkably exaggerated LPS-induced acute lung injury. Molecular studies identified the inflammation repressor suppressor of cytokine signaling (SOCS-1) as the downstream target of miR-155. By binding to the 3′-UTR of the SOCS-1 mRNA, miR-155 downregulated SOCS-1 expression, thus, permitting the inflammatory response during lung injury. Finally, we generated a novel miR-155 knockout rat strain and showed that the proinflammatory role of miR-155 was conserved in rats. Our study identified miR-155 as a proinflammatory factor after LPS stimulation, and alveolar macrophages-derived miR-155 has an important role in LPS-induced ALI.

Effect of continuous hemofiltration on hemodynamics, lung inflammation and pulmonary edema in a canine model of acute lung injury

2003 ◽  
Vol 29 (11) ◽  
pp. 2034-2042 ◽  
Author(s):  
Xiao Su ◽  
Chunxue Bai ◽  
Qunying Hong ◽  
Duming Zhu ◽  
Lixian He ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Pulmonary Edema ◽  
Lung Inflammation ◽  
Canine Model ◽  
Continuous Hemofiltration

scholarly journals GPR84 inhibitor ameliorated lung inflammation and modulated NF-κB through MAPK signalling pathway

2021 ◽  
Author(s):  
Ting Wang ◽  
Yan Zou ◽  
He Lv
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Lung Inflammation ◽  
Cell Model ◽  
Signalling Pathway ◽  
Tunel Staining ◽  
Mapk Signalling Pathway ◽  
Mapk Signalling ◽  
Lps Treatment

Abstract We set our experiments to investigate the role of GPR84 in LPS-induced acute lung injury. The expression of GPR84 was detected through RT-qPCR and Western blotting (WB) after LPS treatment in ALI mouse and cell model, respectively. Following the treatment of GPR 84 inhibitor, the lung injury was evaluated through HE staining while the MAPK signalling components were analyzed through WB, as well as NF-κB signalling components. These components were further analyzed by the addition of anisomycin or TPA. The analysis of apoptosis was performed through TUNEL staining. We showed that LPS stimulated the expression of GPR84 expression. GPR 84 inhibitor facilitated the activation of MAPK signalling while inhibiting MAPK signalling, these effects of which were further rescued by anisomycin or TPA treatment. In conclusion, our findings support that GPR84 inhibitor improved lung injury caused by LPS and revealed a role of GPR87 modulating NF-κB through MAPK signalling pathway. Altogether, GPR84 could be as a prospective target for the treatment of ALI.

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