Neutrophils and acute lung injury

  title={Neutrophils and acute lung injury},
  author={Edward Abraham},
  journal={Critical Care Medicine},
  • E. Abraham
  • Published 1 April 2003
  • Medicine, Biology
  • 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… 
Acute Lung Injury:Apoptosis and Signaling Mechanisms
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.
Contribution of Neutrophils to Acute Lung Injury
This review focuses on the mechanisms of neutrophil recruitment into the lung and on the contribution of Neutrophils to tissue damage in ALI.
Friend or foe? The dual role of neutrophils in lung injury and repair
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.
Epithelial Cell Apoptosis and Neutrophil Recruitment in Acute Lung Injury—A Unifying Hypothesis? What We Have Learned from Small Interfering RNAs
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.
Divergent Effects of Neutrophils on Fas-Induced Pulmonary Inflammation, Apoptosis, and Lung Damage
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.
Role of chemokines in the pathogenesis of acute lung injury.
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.
Divergent Effects of Activated Neutrophils on Inflammation, Kupffer Cell/Splenocyte Activation, and Lung Injury Following Blunt Chest Trauma
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.
The mercurial nature of neutrophils: still an enigma in ARDS?
  • A. WilliamsR. Chambers
  • Medicine, Biology
    American journal of physiology. Lung cellular and molecular physiology
  • 2014
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.
Regulation of inflammation by Rac2 in immune complex-mediated acute lung injury.
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.
Neutrophil alpha-defensins cause lung injury by disrupting the capillary-epithelial barrier.
RATIONALE The involvement of neutrophil activation in the sentinel, potentially reversible, events in the pathogenesis of acute lung injury (ALI) is only partially understood. alpha-Defensins are the


Involvement of Phosphoinositide 3-Kinases in Neutrophil Activation and the Development of Acute Lung Injury1
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.
Neutrophils are major contributors to intraparenchymal lung IL-1 beta expression after hemorrhage and endotoxemia.
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.
Intravascular activation of complement and acute lung injury. Dependency on neutrophils and toxic oxygen metabolites.
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.
Phosphatidic acid signaling mediates lung cytokine expression and lung inflammatory injury after hemorrhage in mice
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.
Proinflammatory activity in bronchoalveolar lavage fluids from patients with ARDS, a prominent role for interleukin-1.
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.
NF-κB Activation Is a Critical Regulator of Human Granulocyte Apoptosis in Vitro*
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.
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 transcriptional
Circulating xanthine oxidase mediates lung neutrophil sequestration after intestinal ischemia-reperfusion.
It is concluded that circulating XO increases acutely and may contribute to pulmonary retention of neutrophils after an ischemic intestinal insult.
Effects of endogenous and exogenous catecholamines on LPS-induced neutrophil trafficking and activation.
The initial accumulation and activation of neutrophils in the lungs after endotoxemia can be significantly diminished by alpha2-adrenergic stimulation, which may have a role in modulating inflammatory pulmonary processes associated with sepsis-induced acute lung injury.
SB 239063, a p38 MAPK inhibitor, reduces neutrophilia, inflammatory cytokines, MMP-9, and fibrosis in lung.
Activity against a range of sequelae commonly associated with COPD and fibrosis is demonstrated, supporting the therapeutic potential of p38 MAPK inhibitors such as SB 239063 in chronic airway disease.