ArticleAmerican journal of respiratory and critical care medicine2009
Antiinflammatory effects of hydrogen peroxide in neutrophil activation and acute lung injury.
Article in American journal of respiratory and critical care medicine, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 96 citations in OpenAlex.
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- Peroxisomes and Kidney Injury.Antioxidants & redox signaling · 2016Review
- Autophagic degradation of peroxisomes in mammals.Biochemical Society transactions · 2016Review
- AMP-Activated Protein Kinase and Glycogen Synthase Kinase 3β Modulate the Severity of Sepsis-Induced Lung Injury.Molecular medicine (Cambridge, Mass.) · 2016Article
- Paradoxical Roles of Antioxidant Enzymes: Basic Mechanisms and Health Implications.Physiological reviews · 2016Review
- The Induction of Pattern-Recognition Receptor Expression against Influenza A Virus through Duox2-Derived Reactive Oxygen Species in Nasal Mucosa.American journal of respiratory cell and molecular biology · 2015Article
- Punicalagin ameliorates lipopolysaccharide-induced acute respiratory distress syndrome in mice.Inflammation · 2015Article
- Endogeous sulfur dioxide protects against oleic acid-induced acute lung injury in association with inhibition of oxidative stress in rats.Laboratory investigation; a journal of technical methods and pathology · 2015Article
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
rationaleAlthough reactive oxygen species (ROS) are generally considered to be proinflammatory and to contribute to cellular and organ dysfunction when present in excessive amounts, there is evidence that specific ROS, particularly hydrogen peroxide (H(2)O(2)), may have antiinflammatory properties.
objectivesTo address the role that increases in intracellular H(2)O(2) may play in acute inflammatory processes, we examined the effects of catalase inhibition or the absence of catalase on LPS-induced inflammatory responses.
methodsNeutrophils from control or acatalasemic mice, or control neutrophils incubated with the catalase inhibitor aminotriazole, were treated with LPS, and levels of reactive oxygen species, proteasomal activity, NF-kappaB activation, and proinflammatory cytokine expression were measured. Acute lung injury (ALI) was produced by intratracheal injection of LPS into control, acatalasemic-, or aminotriazole-treated mice. MEASUREMENTS AND MAIN
resultsIntracellular levels of H(2)O(2) were increased in acatalasemic neutrophils and in neutrophils exposed to aminotriazole. Compared with LPS-stimulated neutrophils from control mice, neutrophils from acatalasemic mice or neutrophils treated with aminotriazole demonstrated reduced 20S and 26S proteasomal activity, IkappaB-alpha degradation, NF-kappaB nuclear accumulation, and production of the proinflammatory cytokines TNF-alpha and macrophage inhibitory protein (MIP)-2. The severity of LPS-induced ALI was less in acatalasemic mice and in mice treated with aminotriazole as compared with that found in control mice.
conclusionsThese results indicate that H(2)O(2) has antiinflammatory effects on neutrophil activation and inflammatory processes, such as ALI, in which activated neutrophils play a major role.
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