Lipopolysaccharide-induced Lung Injury in Mice. I. Concomitant Evaluation of Inflammatory Cells and Haemorrhagic Lung Damage

Asti, Cinzia; Ruggieri, V.; Porzio, S.; Chiusaroli, Riccardo; Melillo, G.; Caselli, Gianfranco

doi:10.1006/pupt.2000.0231

Cited by 96 publications

(54 citation statements)

References 30 publications

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“…In contrast, a significant decrease was observed following LPS challenge only at the earlier time point (4hours). This observation was in agreement with a previous report 41 and probably reflects macrophages adherence to the alveolar surface. Infiltrating neutrophils were also activated after the LPS challenge as evidenced by the increased levels of MPO activity.…”

Section: Discussionsupporting

confidence: 94%

Mechanistic Evaluation of Butea Monosperma Using in Vitro and in Vivo Murine Models of Bronchial Asthma

Shirole¹,

Sutariya²,

Saraf³

2013

Int. J. Res. Ayurveda Pharm.

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The present investigation aimed to elucidate the probable mechanism of antiasthmatic action of Butea monosperma. Bioactive fractionations of methanolic extract of B. monosperma (MBM) were carried out to get, ethyl acetate fraction (EBM) and butanolic fraction (BBM) of Butea monosperma. All fractions were evaluated mechanistically for its antiasthmatic actions in vitro using lipoxygenase assay. The lipoxygenase inhibitory effect of the extract followed the order BBM > MBM > EBM. Based on in vitro lipoxygenase assay BBM was selected for in vitro compound 48/80 induced mast cell degranulation assay and in vivo lipopolysaccharide induced inflammation in rats. BBM 50, 100 and 200μg/ml inhibited compound 48/80 induced mast cell degranulation. BBM exhibited dose dependent (50, 100 and 200mg/kg i.p.) inhibition of lipopolysaccharide-induced increased in total cell count, differential leukocyte count, nitrate-nitrite, total protein and albumin levels in bronchoalveolar fluid (BALF) and myeloperoxidase (MPO) levels in lungs homogenate.

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Section: Discussionsupporting

confidence: 94%

Mechanistic Evaluation of Butea Monosperma Using in Vitro and in Vivo Murine Models of Bronchial Asthma

Shirole¹,

Sutariya²,

Saraf³

2013

Int. J. Res. Ayurveda Pharm.

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“…Interestingly, respiratory mechanics and histological lung changes observed at 24 h were already present as early as 6 h after ALI induction, although less intense. ASTI et al [31] also observed a massive margination of polymorphonuclear cells in lung parenchyma and in the BALF with a similar dose of intratracheal LPS. They demonstrated a significant increase in lung myeloperoxidase activity at 4 h (131% increase versus controls, pv0.001) and 6 h (147% increase versus controls, pv0.001).…”

Section: Discussionmentioning

confidence: 79%

Therapeutic potential of a new phosphodiesterase inhibitor in acute lung injury

Rocco¹,

Momesso²,

Figueira³

et al. 2003

Eur Respir J

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The effects of LASSBio596, a phosphodiesterase type-4 and -5 inhibitor, were tested in Escherichia coli lipopolysaccharide (LPS)-induced acute lung injury.Twenty-four BALB/c mice were randomly divided into four groups. In the control group, saline (0.05 mL) was injected intratracheally (i.t.). The LPS group received LPS (10 mg i.t., 0.05 mL). In the LASSBio596 groups, LASSBio596 (10 mg?kg -1 , 0.2 mL) was injected intraperitoneally 1 h before or 6 h after LPS administration. After 24 h, in vivo (lung resistive and viscoelastic pressures, and static and dynamic elastances) and in vitro (tissue resistance, elastance and hysteresivity) pulmonary mechanics, lung morphometry and collagenous fibre content were computed. Neutrophils and tumour necrosis factor (TNF)-a levels were evaluated in the bronchoalveolar lavage fluid.LASSBio596 prevented the changes in lung mechanics, and inhibited neutrophilic recruitment, TNF-a release, bronchoconstriction, alveolar collapse and the increment of collagen fibre content induced by LPS, independently of the moment of injection.In conclusion, LASSBio596 modulated the lung inflammatory process and had the potential to block fibroproliferation. Thus, agents that inhibit phosphodiesterase 4 and 5 simultaneously may be a useful adjunct therapy for acute lung injury.

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“…15 Briefly, animals were anesthetized with ketamine (30 mg/kg) intraperitoneally (i.p.). Sterile saline solution containing LPS was placed after intubation and aspirated into the lungs (3.0 mg/kg).…”

Section: Animalsmentioning

confidence: 99%

Resolvin D1 reduces deterioration of tight junction proteins by upregulating HO-1 in LPS-induced mice

Xie

Wang

et al. 2013

Laboratory Investigation

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Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) is characterized by increased pulmonary permeability with high mortality. Resolvin D1 (RvD1), which has potent anti-inflammatory and pro-resolving activity, can attenuate pulmonary edema in the animal model of ALI. However, the mechanism underlying the protection of RvD1 on pulmonary edema is still unknown. Here we explore the effects and mechanism of RvD1 on the disruption of tight junction protein that results in the permeability edema in a model of lipopolysaccharide (LPS)-induced ALI. The severity of pulmonary edema was assessed by wet-to-dry rate and Evans blue infiltration; expressions of tight junction (TJ) proteins occludin and zona occludin-1 (ZO-1) were examined by immunofluorescence staining and western blot; mRNA in lung tissue was studied by real time-PCR; the TUNEL kit was performed for the detection of apoptosis of pulmonary barrier. Twenty-four hours after LPS inhalation by mice, wet-to-dry rate and Evans blue infiltration indicated that pretreatment with RvD1 relieved the pulmonary edema and pulmonary capillary permeability. Moreover, RvD1 attenuated the LPS-induced deterioration of TJ protein ZO-1 and occludin significantly. And we found that RvD1 increased heme oxygenase-1 (HO-1) expression contributed to the protection on the deterioration of TJs. In addition, we found that RvD1 could reduce pulmonary cellular apoptosis in LPS-induced mice. In conclusion, RvD1 possesses the ability that relieves the pulmonary edema and restores pulmonary capillary permeability and reduces disruption of TJs in LPS-induced ALI of mice, at least in part, by upregulating HO-1 expression.

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Lipopolysaccharide-induced Lung Injury in Mice. I. Concomitant Evaluation of Inflammatory Cells and Haemorrhagic Lung Damage

Cited by 96 publications

References 30 publications

Mechanistic Evaluation of Butea Monosperma Using in Vitro and in Vivo Murine Models of Bronchial Asthma

Mechanistic Evaluation of Butea Monosperma Using in Vitro and in Vivo Murine Models of Bronchial Asthma

Therapeutic potential of a new phosphodiesterase inhibitor in acute lung injury

Resolvin D1 reduces deterioration of tight junction proteins by upregulating HO-1 in LPS-induced mice

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