Adherent Neutrophils Mediate Permeability After Atelectasis

Goldman, Gideon; Welbourn, Richard; Rothlein, Robert; Wiles, Marc E.; Kobzik, Lester; Valeri, C. R.; Shepro, David; Hechtman, Herbert B.

doi:10.1097/00000658-199209000-00017

Cited by 18 publications

(8 citation statements)

References 35 publications

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“…This leads to an important possibility: increases in protein or PMNs in lavage fluid are not related causally to acute lung injury. This possibility implies that measures of protein or PMNs by bronchoalveolar lavage may have little value in predicting the survival time of patients with acute lung injury, a finding consistent with previous animal studies (12,13,24) and clinical observations (16,40,55).…”

Section: Discussionsupporting

confidence: 68%

Genetic susceptibility to irritant-induced acute lung injury in mice

Wesselkamper

Prows

Biswas

et al. 2000

American Journal of Physiology-Lung Cellular and Molecular Phys

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Recent studies suggest that genetic variability can influence irritant-induced lung injury and inflammation. To begin identifying genes controlling susceptibility to inhaled irritants, seven inbred mouse strains were continuously exposed to nickel sulfate (NiSO(4)), polytetrafluoroethylene, or ozone (O(3)), and survival time was recorded. The A/J (A) mouse strain was sensitive, the C3H/He (C3) strain was intermediate, and the C57BL/6 (B6) strain was resistant to NiSO(4)-induced acute lung injury. The B6AF(1) offspring were also resistant. The strain sensitivity pattern for NiSO(4) exposure was similar to that of polytetrafluoroethylene or ozone (O(3)). Pulmonary pathology was comparable for A and B6 mice. In the A strain, 15 microg/m(3) of NiSO(4) produced 20% mortality. The strain sensitivity patterns for lavage fluid proteins (B6 > C3 > A) and neutrophils (A >/= B6 > C3) differed from those for acute lung injury. This phenotype discordance suggests that these traits are not causally linked (i.e., controlled by independent arrays of genes). As in acute lung injury, B6C3F(1) offspring exhibited phenotypes (lavage fluid proteins and neutrophils) resembling those of the resistant parental strain. Agreement of acute lung injury strain sensitivity patterns among irritants suggested a common mechanism, possibly oxidative stress, and offspring resistance suggested that sensitivity is inherited as a recessive trait.

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Section: Discussionsupporting

confidence: 68%

Genetic susceptibility to irritant-induced acute lung injury in mice

Wesselkamper

Prows

Biswas

et al. 2000

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…Previously proposed mechanisms for the pathogenesis of RPE include changes in surfactant, accumulation of alveolar macrophages and neutrophils, mechanical stress, and production of ROS (10,24,26,30,31,33). That we found BOF-4272 to inhibit ROS production in LBO rats (Fig.…”

Section: Discussionsupporting

confidence: 57%

“…In addition, some evidence suggests changes in alveolar surfactant may contribute to RPE (26,31), and a number of investigators have reported that neutrophil accumulation in the lung induced by various chemokines (e.g., IL-8 and monocyte chemoattractant protein-1), chemical mediators, and adhesion molecules (24,30) plays a major role in RPE (33). Consistent with that idea, it is known that the interaction between adherent neutrophils and endothelial cells regulates lung permeability in RPE (10) and that reactive oxygen species (ROS) produced by neutrophils increase pulmonary endothelial permeability. On the other hand, using an animal RPE model Jackson et al (14) found that exogenous catalase does not prevent RPE, which eliminates extracellular hydrogen peroxide as an important contributor, but they did detect endogenous lung catalase activity and hydrogen peroxide release.…”

mentioning

confidence: 82%

Pulmonary reexpansion causes xanthine oxidase-induced apoptosis in rat lung

Saitô¹,

Ogawa²,

Minamiya³

2005

American Journal of Physiology-Lung Cellular and Molecular Phys

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Saito, Satoshi, Jun-ichi Ogawa, and Yoshihiro Minamiya. Pulmonary reexpansion causes xanthine oxidase-induced apoptosis in rat lung. Am J Physiol Lung Cell Mol Physiol 289: L400 -L406, 2005. First published May 6, 2005; doi:10.1152/ajplung.00136.2005.-The pathogenesis of reexpansion pulmonary edema is not yet fully understood. We therefore studied its mechanism in a rat model in which the left lung was collapsed by bronchial occlusion for 1 h and then reexpanded and ventilated for an additional 3 h. We then evaluated the production of reactive oxygen species in the lungs using fluorescent imaging and cerium deposition electron microscopic techniques and the incidence of apoptosis using the TdT-mediated dUTP-digoxigenin nick end labeling (TUNEL) method. We found that pulmonary reexpansion induced production of reactive oxygen species and then apoptosis, mainly in endothelial and alveolar type II epithelial cells. Endothelial cells and alveolar type I and II epithelial cells in the reexpanded lung were positive for TUNEL and cleaved caspase-3. DNA fragmentation was also observed in the reexpanded lung. In addition, wet-dry ratios obtained with reexpanded lungs were significantly higher than those obtained with control lungs, indicating increased fluid content. All of these effects were attenuated by pretreating rats with a specific xanthine oxidase inhibitor, sodium (Ϫ)-8-(3-methoxy-4-phenylsulfinylphenyl) pyrazolo[1,5-a]-1,3,5-triazine-4(1H)-one. It thus appears that pulmonary reexpansion activates xanthine oxidase in both endothelial and alveolar type II epithelial cells and that the reactive oxygen species produced by the enzyme induce apoptosis among the endothelial and alveolar type I and II epithelial cells that make up the pulmonary water-air barrier, leading to reexpansion pulmonary edema.reactive oxygen species; caspase-3; type II alveolar epithelial cell; reoxygenation REEXPANSION PULMONARY EDEMA (RPE) is a rare complication of the treatment of lung collapse secondary to pneumothorax, pleural effusion, or atelectasis. Although physicians generally believe that, unlike acute respiratory distress syndrome (ARDS), RPE does not require intensive care, the outcome of RPE is reportedly fatal in 20% of patients (17). Moreover, reexpansion after atelectatic storage for hypothermic preservation of lungs before transplantation may be responsible for postpreservation and postreperfusion lung injury (7).The mechanism responsible for RPE is not fully understood. It has been suggested that after atelectasis the mechanical stresses related to lung inflation may cause RPE (28). This effect has also been mentioned as a contributor to the pathogenesis of postpreservation lung injury (9). In addition, some evidence suggests changes in alveolar surfactant may contribute to RPE (26,31), and a number of investigators have reported that neutrophil accumulation in the lung induced by various chemokines (e.g., IL-8 and monocyte chemoattractant protein-1), chemical mediators, and adhesion molecules (24, 30) plays a major role in ...

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“…Reperfusion of the ischemic lower limb is associated with the generation of oxygen-free radicals, which can cause cell membrane damage and increased permeability [30,31]. In addition, these toxic oxygen metabolites activate inflammatory cascades, such as the arachidonic acid cascade, with the production of potent vasoactive and chemoattractant mediators (e.g., thromboxane A 2 and leukotriene B 4 [32,33]). These proinflammatory mediators have been implicated in causing remote lung injury following reperfusion of the acutely ischemic lower limb [30].…”

Section: Discussionmentioning

confidence: 99%

Mortality following Lower Limb Ischemia‐Reperfusion: A Systemic Inflammatory Response?

et al. 1996

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Restoration of blood flow to an acutely ischemic lower limb may paradoxically result in systemic complications and unexpected mortality. It has been suggested that lower limb ischemia reperfusion alters gut permeability. In this study, using a rat model, we determined the effect of acute lower limb ischemia-reperfusion on mortality rate, bowel morphology, and circulating concentrations of endotoxin and the proinflammatory cytokine interleukin-6. Survival rate was compared in two groups of adult Wistar rats: (1) control group (n = 10); and (2) animals subjected to 3 hours of bilateral hind limb ischemia followed by reperfusion (n = 10). Both groups were observed under standard conditions for 4 days. In a second experiment three groups of animals were studied: (I) control (n = 12); (II) 3 hours of bilateral hind limb ischemia alone (n = 12); and (III) 3 hours of bilateral hind limb ischemia followed by 2 hours of reperfusion (n = 12). Animals subjected to bilateral hind limb ischemia followed by reperfusion had a significantly higher mortality rate (70%) than controls (0%) (p < 0.005). Morphometric assessment of the small bowel showed a significant decrease in mean mucosal thickness in the ischemia-reperfusion group compared with that in the group of controls and the ischemia-alone group (p < 0.05). Bilateral hind limb ischemia followed by reperfusion was associated with significantly increased plasma concentrations of endotoxin (p < 0. 05) and interleukin-6 (p < 0.0001) compared with that of controls and ischemia alone. These results indicate that reperfusion of the acutely ischemic lower limb is accompanied by structural changes in the gut mucosa associated with increased systemic endotoxin concentrations and cytokine activation. Mortality following reperfusion of the acutely ischemic limb may be related to a systemic inflammatory response triggered by endotoxin of gut origin.

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Adherent Neutrophils Mediate Permeability After Atelectasis

Cited by 18 publications

References 35 publications

Genetic susceptibility to irritant-induced acute lung injury in mice

Genetic susceptibility to irritant-induced acute lung injury in mice

Pulmonary reexpansion causes xanthine oxidase-induced apoptosis in rat lung

Mortality following Lower Limb Ischemia‐Reperfusion: A Systemic Inflammatory Response?

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