Metalloproteinase inhibition reduces lung injury and improves survival after cecal ligation and puncture in rats

Steinberg, Jay; Halter, Jeffrey; Schiller, Henry J.; DaSilva, Marcelo C.; Landas, Steve K.; Gatto, Louis A.; Maisi, Päivi; Sorsa, Timo; Rajamäki, Minna; Lee, Hsi‐Ming; Nieman, Gary F.

doi:10.1016/s0022-4804(03)00089-1

Cited by 89 publications

(72 citation statements)

References 51 publications

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“…A close association has been described between lung expression of Mmp9 and early alveolar remodeling in acute lung injury (1,12,20), and Mmp9-knockout mice show decreased acute lung injury. This evidence indicates that the role of MMP-9 is not limited to the ability to break down ECM but is also extended to the modulation of cytokines such as IL-1 and IL-6 as well as to leukocyte migration (27,29,39). In addition, therapies aimed at reducing MMP-9 have been correlated with improved survival of mice exposed to acute lung injury (29).…”

Section: Discussionmentioning

confidence: 99%

Protective effects ofS-nitrosoalbumin on lung injury induced by hypoxia-reoxygenation in mouse model of sickle cell disease

Franceschi

Malpeli²,

Scarpa³

et al. 2006

American Journal of Physiology-Lung Cellular and Molecular Phys

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. We investigated the effects of NO donor on hypoxia-induced acute lung injury that occurs when transgenic sickle cell SAD mice are exposed to chronic hypoxia, a model for lung vasoocclusive sickle cell events. In wild-type and SAD mice, intraperitoneal injection of S-nitrosoalbumin (NO-Alb) produced no significant hematologic changes under room air conditions, whereas it induced mild temporary hypotension and inhibition of platelet aggregation. NO-Alb administration (300 mg/kg ip twice a day, equivalent to 7.5 M NO) in wild-type and SAD mice exposed to 46 h of hypoxia (8% oxygen) followed by 2 h of normoxia resulted in 1) reduction of the hypoxiainduced increase in blood neutrophil count, 2) prevention of hypoxiainduced increased IL-6 and IL-1␤ levels in bronchoalveolar lavage, 3) reduction of the lung injury induced by hypoxia-reoxygenation, 4) prevention of thrombus formation, and 5) prevention of hypoxiainduced increase of lung matrix metalloproteinase-9 gene expression. These effects provide new insights into the possible use of NO-Alb in the treatment of acute lung injury in SCD. transgenic sickle cell SAD mice; hypoxic lung injury; nitric oxide; nitrite NITRIC OXIDE (NO) is a potent vasodilator, an inhibitor of vascular remodeling, and a modulator of the cascade of events involved in leukocyte, platelet, and endothelial activation (8,9,21). Sickle cell disease patients show reduced NO metabolites during either vasoocclusive crisis associated with severe pain or acute chest syndrome as well as a decreased exhaled NO, suggesting a possible role of a relative NO lung deficiency in the pathogenesis of sickle cell-related pulmonary complications (25).

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Section: Discussionmentioning

confidence: 99%

Protective effects ofS-nitrosoalbumin on lung injury induced by hypoxia-reoxygenation in mouse model of sickle cell disease

Franceschi

Malpeli²,

Scarpa³

et al. 2006

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…[11][12][13][14] Adhesion formation is associated with significant oxidative stress, both from the activation of the mesothelium and underlying endothelial cells and, more importantly, from the infiltration and subsequent activation of neutrophils and macrophages and cytokines. [15][16][17] Methylene blue (MB) acts as an antioxidant and may reduce intraabdominal nascent fibrinous adhesions, and is rapidly degraded via intraabdominal proteases such as tissue plasminogen activator (tPA), which is a major component of the peritoneal fibrinolytic system. [16] MB was defined as an effective agent to avoid the permanent fibrous adhesion formation in peritoneal trauma due to antioxidant activity.…”

Section: Methodsmentioning

confidence: 99%

The effects of methylene blue on adhesion formation in a rat model of experimental peritonitis

Kalaycı¹,

Eroğlu²,

Kubilay³

et al. 2011

Ulus Travma Acil Cerrahi Derg

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“…In an indirect model of ALI in rats subjected to CLP, treatment with COL-3 at time of injury showed reduced lung water, improved histological grading for lung injury and increased survival [40]. Importantly, the effect on survival was noted to be more pronounced with further dosing post lung injury [39].…”

Section: Tetracyclinesmentioning

confidence: 96%

Matrix metalloproteinases in acute lung injury: mediators of injury and drivers of repair

Davey¹,

2011

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Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) comprise a spectrum of acute inflammatory pulmonary oedema resulting in refractory hypoxaemia in the absence of an underlying cardiogenic cause. There are multiple pulmonary and extrapulmonary causes and ALI/ARDS patients are a clinically heterogeneous group with associated high morbidity and mortality.Inflammatory injury to the alveolar epithelial and endothelial capillary membrane is a central event in the pathogenesis of ALI/ARDS, and involves degradation of the basement membrane. Matrix metalloproteinases (MMPs) have been implicated in a wide variety of pulmonary pathologies and are capable of degrading all components of the extracellular matrix including the basement membrane and key non-matrix mediators of lung injury such as chemokines and cell surface receptors.While many studies implicate MMPs in the injurious process, there are significant gaps in our knowledge of the role of specific proteases at different phases of injury and repair. This article examines the role of MMPs in injury and repair of the alveolar epithelial-endothelial capillary barrier and discusses the potential for MMP modulation in the prevention and treatment of ALI. The need for further mechanistic and in vivo studies to inform appropriate subsequent clinical trials of MMP modulation will be highlighted. KEYWORDS: Acute lung injury, acute respiratory distress syndrome, extracellular matrix, inflammation, matrix metalloproteinases, repair A cute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are part of a disease spectrum associated with high mortality and considerable morbidity. The most recent diagnostic criteria for ALI/ARDS, developed by the 1994 American-European Consensus Conference Committee [1], are based on the gross clinico-radiological findings; acute onset, bilateral infiltrates on chest radiography, absence of left ventricular failure and the ratio of arterial oxygen tension (Pa,O 2 , expressed in mmHg) to inspired oxygen fraction (FI,O 2 ) measuring ,200 (ARDS) or ,300 (ALI) [2][3][4]. However, ALI/ARDS patients are clinically heterogeneous and this definition does not take into account the underlying aetiology or severity of illness reflected by failure of other organ systems [2]. Irrespective of aetiology, the pathogenesis of ALI/ARDS consists of an excessive and inappropriate inflammatory response to a range of pulmonary or extrapulmonary insults, resulting in damage to the alveolar epithelial-endothelial capillary barrier [3,4]. Clinically, this manifests as refractory hypoxaemia and decreased pulmonary compliance. Pathologically, three phases are recognised: an initial acute inflammatory or exudative phase characterised by

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Metalloproteinase inhibition reduces lung injury and improves survival after cecal ligation and puncture in rats

Cited by 89 publications

References 51 publications

Protective effects ofS-nitrosoalbumin on lung injury induced by hypoxia-reoxygenation in mouse model of sickle cell disease

Protective effects ofS-nitrosoalbumin on lung injury induced by hypoxia-reoxygenation in mouse model of sickle cell disease

The effects of methylene blue on adhesion formation in a rat model of experimental peritonitis

Matrix metalloproteinases in acute lung injury: mediators of injury and drivers of repair

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