Original contributionModulation of the alveolar macrophage respiratory burst by hydroperoxides
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2020, Free Radical Biology and MedicineCitation Excerpt :This complex process involves activation of multiple signaling pathways and production of various mediators including cytokines and oxidants, often referred to by the nonspecific misnomer, reactive oxygen species (ROS). Among these mediators, H2O2 plays a critical role by acting as a signaling messenger to enhance the respiratory burst and activate NF-κB signaling [1–4], and by facilitating the elimination of pathogens [5,6]. Excessive H2O2 and other reactive oxidants however, can exacerbate inflammation and cause oxidative stress [7–10], which is implicated in the pathogenesis of a variety of pathologies, including acute respiratory distress syndrome (ARDS) [11], idiopathic pulmonary fibrosis (IPF) [12,13], and others.
Gene expression and TNF-alpha secretion profile in rainbow trout macrophages following exposures to copper and bacterial lipopolysaccharide
2011, Fish and Shellfish ImmunologyCitation Excerpt :On the other hand, ROS, showing a dual role, are produced by macrophages as cytotoxic agents against pathogens during the respiratory burst, via stimulation of the NADPH oxidase system. Divergent results were reported by Murphy et al. (1995) [19] demonstrating that oxidative stress may depress macrophage function, while Kirkham (2007) [20] stated that macrophages activated under conditions of oxidative stress can generate enhanced inflammatory responses. The present study aimed to evaluate the responses at the level of gene expression including target mRNAs relevant to the activation of immune system (IL-1β, IL-6, TNFα), inflammation (SAA, TCPBP), cell death (caspase 6 and high mobility group box 1–HMGB1), respiratory burst activity (NADPH oxidase) and antioxidant activity (glutathione peroxidase–GPx) of differentiated head kidney macrophages (HKM) to exposure to both copper and LPS, individually and in combination.
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2005, Journal of Biological ChemistryCitation Excerpt :In this model, a transient early agonist-triggered peak of hydrogen peroxide seems essential to sustain oxidase activation, in connection with increased subunit expression (6). On the other hand, while exposure to low hydroperoxide concentrations also stimulates oxidase activity in alveolar macrophages, higher but non-lethal concentrations inhibit the respiratory burst (47). Our finding that PDI clearly associates with oxidase subunits in unstimulated VSMCs is in line with the reported preassembling of p22phox and Nox1/Nox4 in resting cells (3, 4, 25).
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