Leukocyte-derived extracellular superoxide dismutase does not contribute to airspace EC-SOD after interstitial pulmonary injury

Manni, Michelle L.; Epperly, Michael W.; Han, Wei; Blackwell, Timothy S.; Duncan, Steven R.; Piganelli, Jon D.; Oury, Tim D.

doi:10.1152/ajplung.00360.2010

Cited by 4 publications

(4 citation statements)

References 30 publications

(53 reference statements)

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“…Bone marrow chimeras were generated as previously described (30), with eight-week-old wild type or congenic RAGE KO recipient mice receiving 15–20 × 10 6 bone marrow cells in 200 μL Hank’s Buffered Salt Solution by tail vein injection within 8 hours of irradiation. Four weeks following transplantation, mice were given an intratracheal instillation of liposomal encapsulated clodronate to selectively ablate host pulmonary macrophages that survived irradiation (30, 31).…”

Section: Methodsmentioning

confidence: 99%

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Pulmonary receptor for advanced glycation end-products promotes asthma pathogenesis through IL-33 and accumulation of group 2 innate lymphoid cells

Oczypok

Milutinovic

Alcorn

et al. 2015

Journal of Allergy and Clinical Immunology

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Background-Single nucleotide polymorphisms in the human gene for the receptor for advanced glycation end products (RAGE) are associated with an increased incidence of asthma. RAGE is highly expressed in the lung and has been reported to play a vital role in the pathogenesis of murine models of asthma/allergic airway inflammation (AAI) by promoting expression of type 2 cytokines, IL-5 and IL-13. IL-5 and IL-13 are prominently secreted by group 2 innate lymphoid cells (ILC2s), which are stimulated by the pro-allergic cytokine, IL-33.

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Section: Methodsmentioning

confidence: 99%

“…Four weeks following transplantation, mice were given an intratracheal instillation of liposomal encapsulated clodronate to selectively ablate host pulmonary macrophages that survived irradiation (30, 31). By doing so, resident alveolar macrophages can more efficiently repopulate with donor cells after bone marrow transplant.…”

Section: Methodsmentioning

confidence: 99%

Pulmonary receptor for advanced glycation end-products promotes asthma pathogenesis through IL-33 and accumulation of group 2 innate lymphoid cells

Oczypok

Milutinovic

Alcorn

et al. 2015

Journal of Allergy and Clinical Immunology

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“…A likely underlying reason is the heterogeneity of the disease, which might be associated with a direct insult by, e.g., infection, aspiration, or injurious ventilation, or an indirect one during situations of severe systemic inflammation, or, frequently, a combination thereof. Efforts to define endogenous pathways or molecules that protect from ALI have recently significantly contributed to our understanding of ALI pathophysiology (5,36,51,81,95,99,132,150,176,189,226,245,254,256,261). Imai et al (106) were the first to suggest that the signals impacting on the balance between angiotensin converting enzymes (ACE) 1 and 2 modulate the degree of inflammatory lung injury after sepsis, and ACE I/D polymorphism was recently associated with mortality risk of ALI/ ARDS in patients (152).…”

Section: Putative Candidates For Treatment Of Alimentioning

confidence: 99%

Novel concepts of acute lung injury and alveolar-capillary barrier dysfunction

Herold

Gabrielli

Vadász

2013

American Journal of Physiology-Lung Cellular and Molecular Phys

178

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Herold S, Gabrielli NM, Vadász I. Novel concepts of acute lung injury and alveolar-capillary barrier dysfunction. Am J Physiol Lung Cell Mol Physiol 305: L665-L681, 2013. First published September 13, 2013 doi:10.1152/ajplung.00232.2013In this review we summarize recent major advances in our understanding on the molecular mechanisms, mediators, and biomarkers of acute lung injury (ALI) and alveolar-capillary barrier dysfunction, highlighting the role of immune cells, inflammatory and noninflammatory signaling events, mechanical noxae, and the affected cellular and molecular entities and functions. Furthermore, we address novel aspects of resolution and repair of ALI, as well as putative candidates for treatment of ALI, including pharmacological and cellular therapeutic means. alveolar-capillary barrier dysfunction; molecular mechanism; pharmacological and cell-based therapy; pulmonary edema; zaacute lung injury/acute respiratory distress syndrome Immune Cells and Inflammatory Signaling Pathways in ALIOne of the central concepts in acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) is that an unbalanced quantity or quality of the inflammatory response aggravates epithelial or endothelial injury. This includes a dysregulated recruitment of leukocytes and/or an exaggerated activation of these cells; inappropriate expression of cytokines, lipid mediators, or reactive oxygen species; enhanced activation of death receptor signaling (97,98,140,207,240); or an uncontrolled activity of platelets or the coagulation cascade (154). In general, these responses are initiated and maintained by recognition of danger-or pathogen-associated molecular patterns

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“…Thus, alterations to oxidative and inflammatory damage in ALI induced by liver transplantation were focused upon in the present study. The concentrations of H 2 O 2 , MDA and SOD in the lungs subsequent to OALT were determined, which reflects the balance of oxidative stress (21,22). Results indicated a significant increase in the levels of H 2 O 2 and MDA subsequent to OALT, and propofol, NAC and AP pretreatment reduced this increase.…”

Section: Propofol Reduces Lung Water Contentmentioning

confidence: 99%

Propofol alleviates acute lung injury following orthotopic autologous liver transplantation in rats via inhibition of the NADPH oxidase pathway

Luo

Zhu

Yuan

et al. 2014

Molecular Medicine Reports

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Abstract. Acute lung injury (ALI) induced by liver transplantation is detrimental to patient survival, and therapeutic strategies remain limited. Thus, the protective effects of propofol, a commonly used anesthetic with antioxidative and anti-inflammatory properties, were investigated in the present study on ALI induced by orthotopic autologous liver transplantation (OALT). The protective mechanism of propofol was determined to be associated with the inhibition of NADPH oxidase, by comparing its effects with the positive controls apocynin (AP; an NADPH oxidase inhibitor) and N-acegysteine (NAC; a scavenger of reactive oxygen species). The results demonstrated that two proteins (p47phox and gp91phox) of the NADPH oxidase system presented increased expression in rats with ALI induced by OALT, thus leading to increased activation of the oxidative stress and inflammatory reactions. Preconditioning with NAC or AP eliminated this increase, suggesting that antioxidative treatment, particularly with inhibitors of NADPH oxidase, is a promising protective strategy against ALI induced by OALT. Propofol preconditioning at a high (100 mg/kg) or low (50 mg/kg) dose promoted similar protective effects, with the high-dose propofol producing a more marked effect than the low dose. The results suggested that propofol may protect against ALI induced by OALT, the mechanism of which may involve a reduced oxidative stress and inflammatory reaction mediated by NADPH oxidase inhibition.

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Leukocyte-derived extracellular superoxide dismutase does not contribute to airspace EC-SOD after interstitial pulmonary injury

Abstract: Manni ML, Epperly MW, Han W, Blackwell TS, Duncan SR, Piganelli JD, Oury TD. Leukocyte-derived extracellular superoxide dismutase does not contribute to airspace EC-SOD after interstitial pulmonary injury.

Cited by 4 publications

References 30 publications

Pulmonary receptor for advanced glycation end-products promotes asthma pathogenesis through IL-33 and accumulation of group 2 innate lymphoid cells

Pulmonary receptor for advanced glycation end-products promotes asthma pathogenesis through IL-33 and accumulation of group 2 innate lymphoid cells

Novel concepts of acute lung injury and alveolar-capillary barrier dysfunction

Propofol alleviates acute lung injury following orthotopic autologous liver transplantation in rats via inhibition of the NADPH oxidase pathway

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