Neutrophils and acute lung injury

@article{Abraham2003NeutrophilsAA,
  title={Neutrophils and acute lung injury},
  author={Edward Abraham},
  journal={Critical Care Medicine},
  year={2003},
  volume={31},
  pages={S195-S199}
}
  • E. Abraham
  • Published 2003
  • Medicine
  • Critical Care Medicine
ObjectiveNeutrophils are an important component of the inflammatory response that characterizes acute lung injury (ALI). This discussion aims to review the contribution of neutrophils to the development and progression of ALI and to highlight the major intracellular signaling pathways that are involved in neutrophil activation in the setting of ALI. Data SourcesMEDLINE, original research papers, and review papers. Study SelectionRelevant laboratory and clinical studies. Data ExtractionSystemic… Expand
Acute Lung Injury:Apoptosis and Signaling Mechanisms
TLDR
The results support the concept that the upregulation of apoptosis following lung inflammation plays a crucial role in the development of acute lung injury and related disorders such as ARDS. Expand
Contribution of Neutrophils to Acute Lung Injury
TLDR
This review focuses on the mechanisms of neutrophil recruitment into the lung and on the contribution of Neutrophils to tissue damage in ALI. Expand
Friend or foe? The dual role of neutrophils in lung injury and repair
TLDR
The evidence suggests that neutrophils are centrally implicated in the onset and progression of ALI, where endothelial and epithelial injuries are associated with microvascular permeability, increased tissue oedema and an early accumulation of activated neutrophil to the lung. Expand
Epithelial Cell Apoptosis and Neutrophil Recruitment in Acute Lung Injury—A Unifying Hypothesis? What We Have Learned from Small Interfering RNAs
TLDR
The contribution that Fas-mediated inflammation may play as a potential biological link between lung cell apoptosis and PMN recruitment will be considered, as well as the in vivo application of small interfering RNA (siRNA) as a novel approach to the inhibition of ALI and its therapeutic implications. Expand
β-Nitrostyrene derivatives attenuate LPS-mediated acute lung injury via the inhibition of neutrophil-platelet interactions and NET release.
TLDR
New insights are provided for elucidating the complicated regulation of neutrophils and platelets in ALI and sheds further light on future drug development strategies for ALI/ARDS and acute inflammatory diseases. Expand
Divergent Effects of Neutrophils on Fas-Induced Pulmonary Inflammation, Apoptosis, and Lung Damage
TLDR
Neutrophils are a necessary component of Fas-induced lung damage, while not affecting lung apoptosis directly per se, and display higher resistance to Fas-triggered inflammation and apoptosis than AM. Expand
Role of chemokines in the pathogenesis of acute lung injury.
TLDR
Excessive recruitment of leukocytes is critical to the pathogenesis of ALI, and the magnitude and duration of the inflammatory process may ultimately determine the outcome in patients with ALI. Expand
Divergent Effects of Activated Neutrophils on Inflammation, Kupffer Cell/Splenocyte Activation, and Lung Injury Following Blunt Chest Trauma
TLDR
In response to lung trauma, activated neutrophils control inflammation including mediator release from distant immune cells but simultaneously mediate pulmonary tissue damage, which might be a reasonable therapeutic approach in chest trauma–induced lung injury. Expand
The mercurial nature of neutrophils: still an enigma in ARDS?
  • A. Williams, R. Chambers
  • Biology, Medicine
  • American journal of physiology. Lung cellular and molecular physiology
  • 2014
TLDR
Experimental and clinical evidence supporting neutrophils as key players in ARDS and the chemokine network in the inflamed lung is complex and may involve several other chemokines, including CXCL10, CCL2, and CCL7. Expand
Regulation of inflammation by Rac2 in immune complex-mediated acute lung injury.
TLDR
It is proposed that lung injury in response to immune complex deposition is dependent on Rac2 in alveolar macrophages and neutrophils, and that Rac2 is important in mediating lung injury. Expand
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References

SHOWING 1-10 OF 61 REFERENCES
Role of p38 MAP kinase in the development of acute lung injury.
TLDR
Although p38 was activated in lung neutrophils after hemorrhage or endotoxemia, inhibition of p38 did not decrease neutrophil accumulation in the lungs or the development of lung edema under these conditions. Expand
Involvement of Phosphoinositide 3-Kinases in Neutrophil Activation and the Development of Acute Lung Injury1
TLDR
It is found that exposure of neutrophils to endotoxin resulted in phosphorylation of Akt, activation of NF-κB, and expression of the proinflammatory cytokines IL-1β and TNF-α through PI3-K-dependent pathways, and endotoxemia-induced ALI was significantly diminished in mice lacking the p110γ catalytic subunit of PI3 -K. Expand
Neutrophils are major contributors to intraparenchymal lung IL-1 beta expression after hemorrhage and endotoxemia.
TLDR
Data indicate that IL-1beta-producing neutrophils traffic to the lungs rapidly in response to hemorrhage or endotoxemia and support the concept that proinflammatory cytokine production by lung neutrophil may contribute to the development of lung injury after blood loss and sepsis. Expand
Neutrophils as early immunologic effectors in hemorrhage- or endotoxemia-induced acute lung injury.
TLDR
It is shown that neutrophils play a central role in initiating acute inflammatory responses and causing injury in the lungs after hemorrhage or endotoxemia and Neutropenia was associated with significant reductions in IL-1beta and MIP-2 but not in TNF-alpha expression in the lung after endotoxia. Expand
Intravascular activation of complement and acute lung injury. Dependency on neutrophils and toxic oxygen metabolites.
TLDR
These studies suggest that intravascular activation of the complement system leads to neutrophil aggregation and activation, intrapulmonary capillary sequestration of neutrophils, and vascular injury, which may be related to production of toxic oxygen metabolites by complement-activated neutrophILS. Expand
Phosphatidic acid signaling mediates lung cytokine expression and lung inflammatory injury after hemorrhage in mice
TLDR
The results indicate the fundamental role of PA metabolism in the development of acute inflammatory lung injury after blood loss and indicate the need to understand more fully the role of phosphatidic acid pathway signaling in this type of injury. Expand
Proinflammatory activity in bronchoalveolar lavage fluids from patients with ARDS, a prominent role for interleukin-1.
TLDR
Using a bioassay that measures balance of cytokines with their inhibitors, the results indicate that the net proinflammatory activity in ARDS BAL fluids is attributable to IL-1 and not to TNF. Expand
NF-κB Activation Is a Critical Regulator of Human Granulocyte Apoptosis in Vitro*
  • C. Ward, E. Chilvers, +5 authors Adriano G. Rossi
  • Biology, Medicine
  • The Journal of Biological Chemistry
  • 1999
TLDR
Light is shed on the biochemical and molecular mechanisms regulating human granulocyte apoptosis and, in particular, on the transcription factor NF-κB, which plays a crucial role in regulating the physiological cell death pathway in granulocytes. Expand
Role of p38 Mitogen-Activated Protein Kinase in a Murine Model of Pulmonary Inflammation1
TLDR
Results demonstrate a much greater dependence on the p38 MAPK cascade in the neutrophil when compared with other leukocytes, and suggest a means of selectively studying and potentially modulating early inflammation in the lung. Expand
Essential Role of Induced Nitric Oxide in the Initiation of the Inflammatory Response after Hemorrhagic Shock
Resuscitation from hemorrhagic shock induces profound changes in the physiologic processes of many tissues and activates inflammatory cascades that include the activation of stress transcriptionalExpand
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