Enhanced bleomycin-induced pulmonary damage in mice lacking extracellular superoxide dismutase

Fattman, Cheryl L.; Chang, Ling‐Yi; Termin, Toni A; Petersen, Louise Munkhaus; Enghild, Jan J.; Oury, Tim D.

doi:10.1016/s0891-5849(03)00402-7

Cited by 111 publications

(109 citation statements)

References 22 publications

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“…Moreover, the absence of extracellular superoxide dismutase exacerbates conditions that lead to inflammation and pulmonary fibrosis (55). Although these studies suggest that reactive oxygen species contribute to lung damage and fibrosis, they do not clearly indicate the mechanisms of the antioxidant effect.…”

Section: Mmp-12mentioning

confidence: 95%

Role of matrix metalloproteinases in the development of airway inflammation and remodeling

Lagente

Manoury

Nénan

et al. 2005

Braz J Med Biol Res

147

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Section: Mmp-12mentioning

confidence: 95%

Role of matrix metalloproteinases in the development of airway inflammation and remodeling

Lagente

Manoury

Nénan

et al. 2005

Braz J Med Biol Res

147

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“…These results are consistent with those of previous studies that demonstrated that EC-SOD expression in the lung inhibits inflammation in response to a wide variety of pulmonary injuries. [11][12][13]19 …”

Section: Ec-sod Limits Inflammation After E Coli Inoculationmentioning

confidence: 99%

“…EC-SOD is expressed in inflammatory cells 13,19,26 ; however, the subcellular location and function are unknown. In the present study, electron microscopic immunolocalization of EC-SOD in human neutrophils and macrophages in human lung sections revealed that EC-SOD is located in Figure 1.…”

Section: Ec-sod Is Present In Human and Murine Phagocytic Inflammatormentioning

confidence: 99%

“…7 This isozyme of the superoxide dismutase family is highly expressed in the lung and arteries and is bound to the extracellular matrix via its positively charged heparin/matrix-binding domain. [7][8][9][10] EC-SOD acts as both an anti-inflammatory and antifibrotic agent in a number of pulmonary diseases including bleomycin-and asbestos-induced pulmonary fibrosis, [11][12][13][14] hyperoxia, [15][16][17] lipopolysaccharide-induced inflammation, 18 and pulmonary infection. 19,20 One mechanism by which EC-SOD inhibits inflammation is directly binding to and inhibiting oxidative fragmentation of several components in the extracellular matrix including collagen, heparan sulfate, and hyaluronan after interstitial lung injury.…”

mentioning

confidence: 99%

“…In addition to its localization on matrices and in extracellular fluids, EC-SOD is also present intracellularly in neutrophils and macrophages. 13,19,26 However, the local-ization and role of EC-SOD in these inflammatory cells have not been investigated.…”

mentioning

confidence: 99%

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Extracellular Superoxide Dismutase in Macrophages Augments Bacterial Killing by Promoting Phagocytosis

Manni

Tomai

Norris

et al. 2011

The American Journal of Pathology

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Extracellular superoxide dismutase (EC-SOD) is abundant in the lung and limits inflammation and injury in response to many pulmonary insults. To test the hypothesis that EC-SOD has an important role in bacterial infections, wild-type and EC-SOD knockout (KO) mice were infected with Escherichia coli to induce pneumonia. Although mice in the EC-SOD KO group demonstrated greater pulmonary inflammation than did wild-type mice, there was less clearance of bacteria from their lungs after infection. Macrophages and neutrophils express EC-SOD; however, its function and subcellular localization in these inflammatory cells is unclear. In the present study, immunogold electron microscopy revealed EC-SOD in membrane-bound vesicles of phagocytes. These findings suggest that inflammatory cell EC-SOD may have a role in antibacterial defense. To test this hypothesis, phagocytes from wild-type and EC-SOD KO mice were evaluated. Although macrophages lacking EC-SOD produced more reactive oxygen species than did cells expressing EC-SOD after stimulation, they demonstrated significantly impaired phagocytosis and killing of bacteria. Overall, this suggests that EC-SOD facilitates clearance of bacteria and limits inflammation in response to infection by promoting bacterial phagocytosis.

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Oxidative Stress in Pulmonary Fibrosis

Otoupalova

Smith

Cheng

et al. 2020

Comprehensive Physiology

184

104

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Oxidative stress has been linked to various disease states as well as physiological aging. The lungs are uniquely exposed to a highly oxidizing environment and have evolved several mechanisms to attenuate oxidative stress. Idiopathic pulmonary fibrosis (IPF) is a progressive age-related disorder that leads to architectural remodeling, impaired gas exchange, respiratory failure, and death. In this article, we discuss cellular sources of oxidant production, and antioxidant defenses, both enzymatic and nonenzymatic. We outline the current understanding of the pathogenesis of IPF and how oxidative stress contributes to fibrosis. Further, we link oxidative stress to the biology of aging that involves DNA damage responses, loss of proteostasis, and mitochondrial dysfunction. We discuss the recent findings on the role of reactive oxygen species (ROS) in specific fibrotic processes such as macrophage polarization and immunosenescence, alveolar epithelial cell apoptosis and senescence, myofibroblast differentiation and senescence, and alterations in the acellular extracellular matrix. Finally, we provide an overview of the current preclinical studies and clinical trials targeting oxidative stress in fibrosis and potential new strategies for future therapeutic interventions.

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Enhanced bleomycin-induced pulmonary damage in mice lacking extracellular superoxide dismutase

Cited by 111 publications

References 22 publications

Role of matrix metalloproteinases in the development of airway inflammation and remodeling

Role of matrix metalloproteinases in the development of airway inflammation and remodeling

Extracellular Superoxide Dismutase in Macrophages Augments Bacterial Killing by Promoting Phagocytosis

Oxidative Stress in Pulmonary Fibrosis

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