A mouse model of lung injury induced by microbial products: implication of tumor necrosis factor.

Michel, Denis; Liu, Guo-Jian; Widmer, Michael B.; Cantin, André M.

doi:10.1165/ajrcmb.10.6.8003342

Cited by 48 publications

(23 citation statements)

References 34 publications

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“…Thus, we directly administered TNF-␣ by the intranasal route, and we demonstrated that, similarly to LPS exposure, TNF-␣ administration induced airway neutrophilia, enhanced MMP-9 activity, and reduced the IL-10 level in BALF. These results are consistent with data demonstrating that TNF-␣ favored neutrophil sequestration and migration (Ulich et al, 1993;Denis et al, 1994;Goncalves de Moraes et al, 1996) and that the difference in the levels of TNF-␣ and IL-10 modulates cell recruitment. Interestingly, a 30 mg/kg RP 73-401 pretreatment partially but significantly reduced airway neutrophilia and enhanced significantly IL-10 release but did not reduce MMP-9 activity in BAL of TNF-␣-exposed mice.…”

Section: Discussionsupporting

confidence: 92%

The Selective Phosphodiesterase 4 Inhibitor RP 73-401 Reduced Matrix Metalloproteinase 9 Activity and Transforming Growth Factor-β Release During Acute Lung Injury in Mice: The Role of the Balance Between Tumor Necrosis Factor-α and Interleukin-10

Corbel¹,

Germain²,

Lanchou³

et al. 2002

J Pharmacol Exp Ther

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Matrix metalloproteinases (MMPs) and transforming growth factor (TGF)-␤ are involved in airway remodeling associated with the inflammatory process. In this study, we investigated the effect of RP 73-401 (piclamilast), a selective phosphodiesterase-4 inhibitor, on MMP-9 activity and TGF-␤ production in two murine models of acute inflammation. In the first model, the lipopolysaccharide (LPS)-induced increase in neutrophils, MMP-9 activity, and tumor necrosis factor (TNF)-␣ and TGF-␤ release in bronchoalveolar lavage (BAL) was significantly reduced by RP 73-401 pretreatment. In contrast, the BAL interleukin (IL)-10 level was decreased by LPS but restored by RP 73-401. IL-10 administration in LPS-exposed mice elicited a significant reduction in BAL neutrophilia, MMP-9 activity, and TNF-␣ release but not in TGF-␤ production. In the second model, RP 73-401 inhibited BAL neutrophils but not MMP-9 activity and TGF-␤ production that were induced by intranasal TNF-␣. We demonstrated that RP 73-401 might modulate the expression of airway remodeling-associated mediators such as MMP-9 and TGF-␤ and that this effect seemed to be at least partially mediated by the balance between TNF-␣ and IL-10.

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Section: Discussionsupporting

confidence: 92%

The Selective Phosphodiesterase 4 Inhibitor RP 73-401 Reduced Matrix Metalloproteinase 9 Activity and Transforming Growth Factor-β Release During Acute Lung Injury in Mice: The Role of the Balance Between Tumor Necrosis Factor-α and Interleukin-10

Corbel¹,

Germain²,

Lanchou³

et al. 2002

J Pharmacol Exp Ther

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“…Indeed, high levels of TNF-a have been correlated with the severity of pathological disturbances caused by endotoxin (Tracey et al, 1986;Gorgen et al, 1992). Once released, TNF-a favours the migration and sequestration of neutrophils which play a critical role in the pathogenesis of lung inflammation (Ulich et al, 1991;Deni et al, 1994;Steinberg et al, 1994), including adult respiratory distress syndrome (ARDS). The increased adherence of neutrophils to endothelial cells induced by TNF-a leads to their massive infiltration in pulmonary spaces (Albelda et al, 1994;Ulich et al, 1995).…”

Section: Introductionmentioning

confidence: 99%

Effect of cyclo‐oxygenase inhibitors and modulators of cyclic AMP formation on lipopolysaccharide‐induced neutrophil infiltration in mouse lung

Moraes

Vargäftig

Lefort

et al. 1996

British J Pharmacology

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The adult respiratory distress syndrome (ARDS) is an acute lung inflammation developed after direct or indirect contact with pathogenic agents. In the present study, a mouse model was developed to mimic this condition using aerosolized bacterial lipopolysaccharide (LPS) and to investigate the mechanisms involved in the lung inflammatory response. Inhalation of LPS led to a time and dose‐dependent increase in tumour necrosis factor‐α (TNF‐α) production and neutrophil recruitment into the bronchoalveolar lavage fluid (BALF) of Balb/c mice. Under the same conditions, neutrophil infiltration was also found in the BALF of the LPS‐sensitive mouse strain C3H/HeN, but was absent in the LPS‐resistant strain C3H/HeJ. Intranasal administration of murine recombinant TNF‐α also triggered neutrophil recruitment. One hour after inhalation of LPS, half of the maximal level of TNF‐α was measured in the BALF, but only a few neutrophils were detected at this time. The peak TNF‐α concentration was reached at 3 h, when the neutrophil amount started to increase. At 24 h, maximal neutrophil number was found in the BALF and TNF‐α was no longer present. Pretreatment of mice under different experimental conditions demonstrated that: (a) cycloheximide almost completely blocks both neutrophil recruitment and TNF‐α production; (b) anti TNF‐α antibodies block neutrophil recruitment; (c) indomethacin or aspirin enhance by two fold neutrophil recruitment; (d) indomethacin significantly increases TNF‐α production 1 h after inhalation of LPS; (e) dibutyryl cyclic AMP and prostaglandin E2 (PGE2) block both neutrophil recruitment and TNF‐α production. It is concluded that aerosolized LPS in mice triggers an acute lung inflammation which can be used as a potential model of inhalational ARDS and that, strategies leading to the elevation of cyclic AMP levels in vivo can be effective in modulating LPS‐induced TNF‐α synthesis and neutrophil recruitment.

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“…Lipopolysaccharide (LPS), a toxic biological substance that initiates acute inflammation, can produce experimental acute lung injury (ALI) [1][2][3] resulting in hypoxemia. Ongoing exposure to hypoxemia/hypoxia induces death of lung cells, which are vulnerable to hypoxic conditions; hypoxia further increases lung inflammation after LPS exposure.…”

mentioning

confidence: 99%

The 150-Kilodalton Oxygen-Regulated Protein Ameliorates Lipopolysaccharide-Induced Acute Lung Injury in Mice

Nakagomi

Kitada

Kuribayashi

et al. 2004

The American Journal of Pathology

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The 150-kd oxygen-regulated protein is a novel stress protein that is located in the endoplasmic reticulum and contributes to cell survival when this organelle is under stress. Expression of this protein was strongly increased in alveolar macrophages and alveolar epithelial cells from mice with acute lung injury induced by lipopolysaccharide. Transgenic mice overexpressing the 150-kd protein showed decreased histological severity of this lung injury, accompanied by lower total protein concentrations, and lactate dehydrogenase activity in bronchoalveolar lavage fluid. As indicated by nick end-labeling, lipopolysaccharide induced apoptosis in fewer alveolar wall cells in transgenic than in wild-type mice. Transgenic mice also showed increased survival after lipopolysaccharide injection (a log-rank test). Thus, the 150-kd protein, an endoplasmic reticulum-related molecular chaperone, is pivotal in resisting acute lung injury from lipopolysaccharide. Lipopolysaccharide (LPS), a toxic biological substance that initiates acute inflammation, can produce experimental acute lung injury (ALI) 1-3 resulting in hypoxemia. Ongoing exposure to hypoxemia/hypoxia induces death of lung cells, which are vulnerable to hypoxic conditions; hypoxia further increases lung inflammation after LPS exposure.4,5 Thus, hypoxia may play a central role in LPS-induced ALI.Extreme hypoxia induces changes in cellular metabolic homeostasis. The 150-kd oxygen-regulated protein (ORP150/HSP12A), first cloned from cultured astrocytes under hypoxic conditions, 6 is a molecular chaperone belonging to the heat shock protein (HSP) family. Located in the endoplasmic reticulum (ER), ORP150 resembles glucose-regulated proteins (GRPs) such as GRP78 and GRP94. 7 ORP150 expression is required for cells to survive hypoxic conditions, indicating that ORP150 is important in protection of cells from hypoxia/ischemia. 8 In the central nervous system, ORP150 overexpression was found to protect neurons from ischemia by suppression of apoptosis 9 and/or activation of Ca 2ϩ -dependent proteinases. 10,11 These findings establish an important role for this ER-located molecular chaperone in neuronal defense mechanisms against environmental stress.Although ORP150 normally is expressed in most tissues, its role in the development of respiratory diseases has not been evaluated. Severity of ALI is associated with degree of alveolar epithelial cell injury.12 As alveolar epithelial cells participate in essential functions including gas exchange, they must be protected from environmental stresses including hypoxia. Thus, understanding of cellular defense mechanisms against such events could lead to therapeutic strategies that enhance protection of alveolar epithelial cells from pathogenetic insults. Induction of ER-associated chaperones such as ORP150 has not been studied in the respiratory system as a possible mechanism for cytoprotection.We used a mouse model of LPS-induced ALI to examine changes in expression of ORP150 by alveolar epithelial cells, and to determine whether OR...

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A mouse model of lung injury induced by microbial products: implication of tumor necrosis factor.

Cited by 48 publications

References 34 publications

The Selective Phosphodiesterase 4 Inhibitor RP 73-401 Reduced Matrix Metalloproteinase 9 Activity and Transforming Growth Factor-β Release During Acute Lung Injury in Mice: The Role of the Balance Between Tumor Necrosis Factor-α and Interleukin-10

The Selective Phosphodiesterase 4 Inhibitor RP 73-401 Reduced Matrix Metalloproteinase 9 Activity and Transforming Growth Factor-β Release During Acute Lung Injury in Mice: The Role of the Balance Between Tumor Necrosis Factor-α and Interleukin-10

Effect of cyclo‐oxygenase inhibitors and modulators of cyclic AMP formation on lipopolysaccharide‐induced neutrophil infiltration in mouse lung

The 150-Kilodalton Oxygen-Regulated Protein Ameliorates Lipopolysaccharide-Induced Acute Lung Injury in Mice

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