The Modern Version of Adult Respiratory Distress Syndrome

Demling, M.D. Robert H.

doi:10.1146/annurev.med.46.1.193

Cited by 91 publications

(39 citation statements)

References 16 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In order to test this hypothesis, the effect of taxol in a murine model of endotoxin-induced lung injury was examined. Endotoxin/lipopolysaccharide (LPS), a key constituent of Gram-negative bacterial cell walls, is a pro-inflammatory mediator and, when delivered intratracheally, reproducibly displays key features of microvascular lung injury, including leukocyte accumulation in lung tissue, pulmonary oedema, profound lung inflammation and mortality [7,8]. LPS treatment leads to disruption of peripheral microtubules in pneumocytes [9] and vascular endothelial cells [10].…”

mentioning

confidence: 99%

Suppression of endotoxin-induced inflammation by taxol

Mirzapoiazova¹,

Kolosova²,

Moreno³

et al. 2007

Eur Respir J

View full text Add to dashboard Cite

The pathogenesis of acute lung injury includes transendothelial diapedesis of leukocytes into lung tissues and disruption of endothelial/epithelial barriers leading to proteinrich oedema. In vitro studies show that the microtubule network plays a role in the regulation of endothelial permeability as well as in neutrophil locomotion. It was hypothesised that the microtubule-stabilising agent, taxol, might attenuate inflammation and vascular leak associated with acute lung injury in vivo.The effect of intravenously delivered taxol was assessed using a model of murine lung injury induced by intratracheal lipopolysaccharide (LPS) administration. Parameters of lung injury and inflammation were assessed 18 h after treatment.Intravenously delivered taxol significantly reduced inflammatory histological changes in lung parenchyma and parameters of LPS-induced inflammation: infiltration of proteins and inflammatory cells into bronchoalveolar lavage fluid, lung myeloperoxidase activity, and extravasation of Evans blue-labelled albumin into lung tissue. Taxol alone (in the absence of LPS) had no appreciable effect on these parameters. In addition to lung proteins, intravenous taxol reduced accumulation of leukocytes in ascitic fluid in a model of LPS-induced peritonitis.Taken together, the present data demonstrate that microtubule stabilisation with taxol systemically attenuates lipopolysaccharide-induced inflammation and vascular leak.

show abstract

mentioning

confidence: 99%

Suppression of endotoxin-induced inflammation by taxol

Mirzapoiazova¹,

Kolosova²,

Moreno³

et al. 2007

Eur Respir J

View full text Add to dashboard Cite

show abstract

“…In particular, cytokines, chemokines and reactive oxygen species (ROS) have been implicated. Cytokines and chemokines, which are both produced as part of the host immune response to bacteria (1-2), contribute to the pathogenesis of tissue damage (3)(4). ROS contributes to the antibacterial response, even if overproduction can result in oxidative stress that amplifies the inflammatory response.…”

mentioning

confidence: 99%

N-Acetylcysteine Synergizes with Oseltamivir in Protecting Mice from Lethal Influenza Infection

Garozzo

Tempera

Ungheri

et al. 2007

Int J Immunopathol Pharmacol

View full text Add to dashboard Cite

Many studies have shown that oxidative stress is important in the pathogenesis of pulmonary damage during influenza virus infections. Antioxidant molecules are therefore potentially useful against viral infection. Our previous studies show that N-acetylcysteine (NAC) has a protective effect in a model of lethal influenza infection in mice. NAC administration significantly decreased the mortality in infected mice. Further studies have demonstrated that NAC enhanced survival in combination with the antiviral agent ribavirin. In the present study, we report the effect of combined treatment with NAC and Oseltamivir, clinically used in the treatment and prevention of influenza virus infection, in a murine model of lethal influenza infection. NAC was given as a single daily dose of 1000 mg/Kg starting from 4 h before infection and until day 4 after infection; Oseltamivir was given twice daily at dose of 1 mg/Kg/die for 5 days, starting from 4 h before infection. End-point evaluation was 21-days' survival. NAC alone was slightly effective (20%), since a suboptimal treatment was used. Survival increased to 60% with Oseltamivir and to 100% with Oseltamivir and NAC used in combination. Since NAC alone does not show any antiviral action, the present findings suggest that antioxidant therapy increase survival by an improvement in host defense mechanisms, and/or by a direct antioxidant effect against oxidative stress associated with viral infection. Our studies demonstrate the effectiveness of combining agents acting through different mechanisms, such as antiviral drugs oseltamivir and the antioxidant NAC, indicating a possible advantage of combining the two treatments.

show abstract

“…T he acute respiratory distress syndrome (ARDS) 4 has been defined as a severe form of acute lung injury featuring pulmonary inflammation and increased capillary leak (1). ARDS is associated with a high mortality rate and accounts for Ͼ100,000 deaths annually in the United States (2).…”

mentioning

confidence: 99%

“…ARDS may arise in a number of clinical situations, especially in patients with sepsis (3). A well-described pathophysiological model of ARDS is one form of the acute lung inflammation mediated by neutrophils, cytokines, and oxidant stress (4).…”

mentioning

confidence: 99%

Divergent Signaling Pathways in Phagocytic Cells during Sepsis

Guo

Riedemann

Sun

et al. 2006

The Journal of Immunology

View full text Add to dashboard Cite

Neutrophil accumulation in the lung plays a pivotal role in the pathogenesis of acute lung injury during sepsis. Directed movement of neutrophils is mediated by a group of chemoattractants, especially CXC chemokines. Local lung production of CXC chemokines is intensified during experimental sepsis induced by cecal ligation and puncture (CLP), as reflected by rising levels of MIP-2 and cytokine-induced neutrophil chemoattractant-1 in bronchoalveolar lavage fluids. Alveolar macrophages are primed and blood neutrophils are down-regulated for production of MIP-2 and cytokine-induced neutrophil chemoattractant production in response to LPS and C5a. Under these conditions of stimulation, activation of MAPKs (p38, p42/p44) occurs in sham neutrophils but not in CLP neutrophils, while under the same conditions phosphorylation of p38 and p42/p44 occurs in both sham and CLP alveolar macrophages. These data indicate that, under septic conditions, there is impaired signaling in neutrophils and enhanced signaling in alveolar macrophages, resulting in CXC chemokine production, and C5a appears to play a pivotal role in this process. As a result, CXC chemokines increase in lung, setting the stage for neutrophil accumulation in lung during sepsis.

show abstract

The Modern Version of Adult Respiratory Distress Syndrome

Cited by 91 publications

References 16 publications

Suppression of endotoxin-induced inflammation by taxol

Suppression of endotoxin-induced inflammation by taxol

N-Acetylcysteine Synergizes with Oseltamivir in Protecting Mice from Lethal Influenza Infection

Divergent Signaling Pathways in Phagocytic Cells during Sepsis

Contact Info

Product

Resources

About