Endotoxin-stimulated alveolar macrophage recruitment of neutrophils and modulation with exogenous surfactant

Finck, Christine; Hodell, M; Marx, William; Paskanik, Andrew M.; McGraw, Daniel J.; Lutz, Charles J.; Gatto, Louis A.; Picone, Anthony; Nieman, Gary F.

doi:10.1097/00003246-199808000-00029

Cited by 16 publications

(9 citation statements)

References 24 publications

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“…The alveolar wall reacts with hyperplasia of type-II pneumocytes and hypertrophy of fibroblastic interstitial cells [3,4]. The morphological findings on mononuclear phagocyte infiltration into the lung parenchyma preceding that of neutrophils is in agreement with more recent data on primary stimulation of mononuclear phagocytes by LPS leading to secretion of neutrophil chemoattractant cytokines [5][6][7].…”

Section: Introductionsupporting

confidence: 82%

Evolution of Endotoxin-Induced Lung Injury in the Rat beyond the Acute Phase

Domenici

Pieri²,

Gallè³

et al. 2004

Pathobiology

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Objectives: Intratracheal endotoxin in rats causes acute lung injury. Here we have addressed the cellular physiopathology of lung recovery from that injury. Methods: The lungs of 5 untreated rats and rats treated with intratracheal endotoxin from 2, 3, 5, 8 (5 rats each) and 15 days (2 rats) were studied by light and electron microscopy and immunohistochemistry. Results: In the acute phase there was a reduction in the aerated spaces (p < 0.01); diffuse infiltration of granulocytes and macrophages; hyperplasia of type-II pneumocytes, and hypertrophy of interstitial cells. Aerated spaces improved during recovery. In the early recovery phase (3–8 days) the compartmentalization of infiltrating cells varied significantly (p < 0.01): macrophages remained widespread while neutrophils were inside blood vessels. Many pneumocytes were intermediate between type-I and type-II cells. In the late recovery phase (15 days) the infiltrate disappeared; myofibroblasts were significantly more than previously (p < 0.01) and extracellular matrix was abundant; type-II pneumocytes contained non-lamellated lipid inclusions. Conclusions: Macrophages play a pivotal role in the damage-repair processes of the lung following endotoxin injury, leading to an increase in extracellular matrix, differentiation of myofibroblasts and altered secretion of surfactant by newly differentiated type-II pneumocytes.

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Section: Introductionsupporting

confidence: 82%

Evolution of Endotoxin-Induced Lung Injury in the Rat beyond the Acute Phase

Domenici

Pieri²,

Gallè³

et al. 2004

Pathobiology

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“…Both colfosceril and beractant inhibited cytokine secretion by Staphylococcus aureus, and interleukin-1 [13]. Calfactant has also been shown to alter the chemotactic migration of neutrophils toward LPSstimulated AMs, suggesting an inhibition of chemokine secretion and beractant suppresses expression and secretion of the chemokine MIP-1α in human AMs [4,21].…”

Section: Lps + Beractantmentioning

confidence: 98%

“…Natural surfactant isolates inhibit macrophage-mediated neutrophil chemotaxis [4], nitric oxide (NO) production [5], and oxidative burst activity [6]. Natural surfactant's hydrophilic proteins (surfactant protein-A and -D) have been shown to mediate host defense properties [7,8].…”

Section: Introductionmentioning

confidence: 99%

Immunosuppressive properties of surfactant in alveolar macrophage NR8383

et al. 2008

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Exogenous surfactants and surfactant phospholipid inhibit secretion of proinflammatory cytokines and NO in NR8383 AMs. The inhibitory effects of beractant on oxygen radical and LPS-induced NO formation may result from unique mechanisms of decreasing cell signaling. The anti-inflammatory activity of surfactant products used in the treatment of neonatal respiratory distress syndrome (RDS) may depend upon the specific preparation or dose used.

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“…It has been demonstrated that natural surfactant can modulate the pulmonary inflammatory cascade by inhibiting macrophage-mediated neutrophil chemotaxis [7], nitric oxide production [8], oxidative burst activity [9], and secretion of proinflammatory cytokines from alveolar macrophages [10]. In addition, glucocorticoids have been shown to decrease oxidative stress in lungs in the presence of inflammation [11,12,13,14].…”

Section: Introductionmentioning

confidence: 99%

Natural Surfactant Combined with Beclomethasone Decreases Lung Inflammation in the Preterm Lamb

et al. 2011

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Background: Natural surfactant combined with beclomethasone decreases pulmonary oxidative stress in preterm lambs with respiratory distress syndrome (RDS). Objectives: To test the hypothesis that this occurs through a decrease in pulmonary inflammation. Methods: Preterm lambs received 200 mg/kg of natural surfactant or 200 mg/kg of natural surfactant combined with 400 or 800 µg/kg of beclomethasone. Interleukin 8 (IL-8) and macrophage migration inhibitory factor (MIF) were assayed in bronchial aspirate samples and lung mechanics were evaluated. Results: IL-8 increased in all the groups, but the increase was lower in the groups treated with surfactant plus 400 and 800 µg/kg of beclomethasone. MIF decreased in the surfactant group, did not vary in the surfactant plus 400 µg/kg beclomethasone group, and decreased in the surfactant plus 800 µg/kg beclomethasone group. MIF concentration was higher in the surfactant plus 800 µg/kg beclomethasone group than in the other groups. Conclusions: Natural surfactant combined with beclomethasone at 800 µg/kg is effective in reducing lung inflammation in an animal model of RDS, thus explaining the associated decrease in lung oxidative stress. The increase in MIF in animals treated with surfactant plus 800 µg/kg of beclomethasone might be an important maturative and protective factor for neonatal lungs.

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Endotoxin-stimulated alveolar macrophage recruitment of neutrophils and modulation with exogenous surfactant

Cited by 16 publications

References 24 publications

Evolution of Endotoxin-Induced Lung Injury in the Rat beyond the Acute Phase

Evolution of Endotoxin-Induced Lung Injury in the Rat beyond the Acute Phase

Immunosuppressive properties of surfactant in alveolar macrophage NR8383

Natural Surfactant Combined with Beclomethasone Decreases Lung Inflammation in the Preterm Lamb

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