Neutrophil activation and acute lung injury

@article{Lee2001NeutrophilAA,
  title={Neutrophil activation and acute lung injury},
  author={Warren L. Lee and Gregory P. Downey},
  journal={Current Opinion in Critical Care},
  year={2001},
  volume={7},
  pages={1-7}
}
  • Warren L. Lee, G. Downey
  • Published 2001
  • Medicine
  • Current Opinion in Critical Care
Neutrophils are considered to be central to the pathogenesis of most forms of acute lung injury (ALI). For the sake of clarity, neutrophil involvement in ALI can be conceptualized as consisting of sequential stages, beginning with their sequestration in the pulmonary microvasculature, followed by adhesion and activation, and culminating in the production of a microbicidal or “effector” response, such as the generation of reactive oxygen species or release of proteolytic enzymes. Great strides… Expand
Inflammatory pathways and microvascular responses in the lung.
  • W. Kuebler
  • Medicine
  • Pharmacological reports : PR
  • 2005
TLDR
The pulmonary microvascular endothelium plays a key role in regulating not only sequestration and emigration of neutrophils, but by initiating the inflammatory response to a variety of diverse stimuli. Expand
With Friends Like These: The Complex Role of Neutrophils in the Progression of Severe Pneumonia
TLDR
The complex role of neutrophils during severe pneumonia is reviewed by highlighting specific molecules and processes that contribute to pulmonary immunity, but can also drive progression of severe disease. Expand
The role of apoptosis in the pathophysiology of Acute Respiratory Distress Syndrome (ARDS): an up-to-date cell-specific review.
TLDR
Evidence is given that TNF-alpha, IL-1beta and IL-13 attenuate the pro-cell death effects of Fas/CD95 on A549 epithelial cells, at least partially, by the NF-kB and PI3-K pathways, suggesting that induction of the expression of antiapoptotic genes protects the epithelium from cell death. Expand
Cyclooxygenase-2 suppresses polymorphonuclear neutrophil apoptosis after acute lung injury.
TLDR
Up-regulation of intrapulmonary COX-2 expression contributes to the suppression of PMN apoptosis after ALI, and apoptosis of normal PMNs was significantly decreased by the addition of BALFALI. Expand
Proteases and lung injury
TLDR
Although the data support a key role for neutrophil elastase in the pathogenesis of ARDS, further study is needed to fully define the actions of neutrophils, and how these actions affect host functions, before the authors can exploit this knowledge for therapeutic benefit. Expand
Alveolar Macrophage Chemokine Secretion Mediates Neutrophilic Lung Injury in Nox2-Deficient Mice
TLDR
It is speculated that Nox2 represses the development of inflammatory lung injury by modulating chemokine expression by the alveolar macrophage. Expand
Injury and repair in lung and airways.
TLDR
The rodent bleomycin model of lung fibrosis allows the use of molecular tools to dissect the cellular and subcellular processes leading to fibrosis and the elements of this response may provide therapeutic targets for the prevention of this devastating complication of ALI/ARDS. Expand
Pathophysiological Approaches of Acute Respiratory Distress syndrome: Novel Bases for Study of Lung Injury
TLDR
These experimental animal models reproduce key components of the injury and resolution phases of human ALI/ARDS and provide a methodology to explore mechanisms and potential new therapies. Expand
A new understanding of pancreatitis-associated pulmonary injury
TLDR
Potential mechanisms of endothelial barrier dysfunction, neutrophil and monocyte/macrophage activation, adhesion molecule expression, initial factors, mast cell involvement and intracellular signaling in PALI are explored. Expand
Inflammatory and Fibrinolytic System in Acute Respiratory Distress Syndrome
TLDR
This review highlights the research evidence of apoptosis and EMT in lung development, injury and its prognosis in ARDS thereby to develop an effective strategy for the treatment of ARDS. Expand
...
1
2
3
4
5
...

References

SHOWING 1-10 OF 78 REFERENCES
Absence of inflammatory lung injury in rabbits challenged intravascularly with complement-derived chemotactic factors.
TLDR
The studies suggest that changes in lung function after ZAP instillation may not represent changes from complement activation alone in that they are not reproduced with CVF or rabbit C5a. Expand
Role of L-selectin in leukocyte sequestration in lung capillaries in a rabbit model of endotoxemia.
TLDR
It is concluded that L-selectin-mediated leukocyte/endothelial interaction is a necessary prerequisite for leukocytes sequestration in alveolar capillaries in this model of acute endotoxemia. Expand
Impaired immunity and enhanced resistance to endotoxin in the absence of neutrophil elastase and cathepsin G.
TLDR
The data demonstrate a critical role of the nonoxidative effector mechanisms of neutrophils in host immunity and immunopathology and identify elastase and cathepsin G as effectors in the endotoxic shock cascade downstream of TNFalpha. Expand
Leukotoxin and its diol induce neutrophil chemotaxis through signal transduction different from that of fMLP.
TLDR
Both leukotoxin and its diol metabolite induce chemotaxis in human neutrophils in a unique way and may act as important bioactive lipids when considering the pathological mechanism of acute lung injury. Expand
Mice lacking neutrophil elastase reveal impaired host defense against gram negative bacterial sepsis
TLDR
It is shown that NE−/− mice are more susceptible than their normal littermates to sepsis and death following intraperitoneal infection with Cram negative (Klebsiella pneumoniae and Escherichia coli) but not Cram positive (Staphylococcus aureus) bacteria. Expand
Resistance to endotoxic shock and reduced neutrophil migration in mice deficient for the Src-family kinases Hck and Fgr.
  • C. Lowell, G. Berton
  • Biology, Medicine
  • Proceedings of the National Academy of Sciences of the United States of America
  • 1998
TLDR
It is demonstrated that defective integrin signaling in neutrophils, caused by loss of Hck and Fgr tyrosine kinase activity, results in impaired inflammation-dependent tissue injury in vivo. Expand
Delayed neutrophil elastase inhibition prevents subsequent progression of acute lung injury induced by endotoxin inhalation in hamsters.
TLDR
It is concluded that delayed inhibition of NE activity with sivelestat prevents subsequent progression of ALI in hamsters after ET inhalation, suggesting that NE may play an important role in the progression of acute lung injury. 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
Matrix metalloproteinase inhibitor prevents acute lung injury after cardiopulmonary bypass.
TLDR
It is suggested that strategies to combat ARDS should target terminal neutrophil effectors, as all pathological changes typical of ALI after CPB were prevented by CMT-3. Expand
Antibody to E- and L-selectin does not prevent lung injury or mortality in septic baboons.
TLDR
It is concluded that treatment with an antibody to E- and L-selectin in gram-negative sepsis does not improve gas exchange or protect against lung injury, and is associated with decreased survival time in primates. Expand
...
1
2
3
4
5
...