Comparative EPR study of different macrophage types stimulated for superoxide and nitric oxide production

Deschacht, Maartje; Horemans, Tessa; Martinet, Wim; Bult, Hidde; Maes, Louis; Cos, Paul

doi:10.3109/10715761003782288

Cited by 15 publications

(18 citation statements)

References 42 publications

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“…Although LPS is known to stimulate ROS production in neutrophils, the reports of LPS-induced ROS generation in macrophages have been controversial in the literature (Szefler et al, 1989;Pfeiffer et al, 2007;Deschacht et al, 2010;Maeda et al, 2010). In contrast, zymosan consistently stimulates ROS generation in macrophages (Russwurm et al, 1994;Bramble and Anderson, 1998) and thus was used as a positive ROS stimulus in our studies.…”

Section: Resultsmentioning

confidence: 58%

Pivotal Role of Reactive Oxygen Species in Differential Regulation of Lipopolysaccharide-Induced Prostaglandins Production in Macrophages

Zhao

Deng

et al. 2012

Mol Pharmacol

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Gram-negative bacterial endotoxin lipopolysaccharide (LPS) triggers the production of inflammatory cytokines, reactive oxygen species (ROS), and prostaglandins (PGs) by pulmonary macrophages. Here, we investigated if ROS influenced PGs production in response to LPS treatment in mouse bone marrow-derived macrophages (BMDM). We observed that pretreatment of BMDM with two structurally unrelated ROS scavengers, MnTMPyP and EUK-134, not only prevented LPS-induced ROS accumulation, but also attenuated the LPS-induced PGD 2 , but not PGE 2 , production. Conversely

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Section: Resultsmentioning

confidence: 58%

Pivotal Role of Reactive Oxygen Species in Differential Regulation of Lipopolysaccharide-Induced Prostaglandins Production in Macrophages

Zhao

Deng

et al. 2012

Mol Pharmacol

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“…The EPR method for the detection of the overall O 2 ●− and NO production in infected and non-infected macrophages was used as described earlier (Deschacht et al 2010). PMM were grown in 24-well plates (Greiner) at 1 × 10 6 cells/well 2 days prior to the test.…”

Section: Methodsmentioning

confidence: 99%

Role of oxidative stress and apoptosis in the cellular response of murine macrophages uponLeishmaniainfection

et al. 2012

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SUMMARYLeishmaniaparasites are able to survive in the macrophage, one of the most hostile environments of the vertebrate host. The present study investigated howLeishmaniainfection influences these host cell defence mechanisms. Macrophages were infected with antimony-susceptible and -resistantLeishmaniastrains. Free radical production inLeishmania-infected macrophages was measured by electron paramagnetic resonance. Apoptosis was detected with fluorescence microscopy using Annexin-V FITC labelling and with Western blotting to detect caspase-3 cleavage. Independent of their drug susceptibility profile or species background, all studiedLeishmaniastrains induced a similar increase in free radical production in macrophages. O2●−production was significantly elevated during phagocytosis of the stationary phase promastigotes. Conversely, NO levels increased later in the infection and none of the strains induced capsase-3 cleavage.Leishmania donovaniinfection led to phosphatidylserine externalization only in RAW 264.7 cells. After an initial burst of O2●−during phagocytosis of promastigotes, amastigotes protect themselves by decreasing the O2●−production to the basal level. An increased NO production was observed 6 h after infection. Finally, induction of cell death is probably not essential in the survival of the parasite within the macrophage.

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“…We examined the effect of cysteamine on extracellular ROS generation in PMAstimulated RAW macrophages using the well established chemiluminescence assay. 21,22 Cysteamine reduced ROS generation by 33% in PMA-stimulated macrophages ( Figure 6A). Because the phagocytosis of apoptotic cells is an important inherent function of macrophages, we measured intracellular oxidant generation in macrophages cocultured with apoptotic renal tubular cells.…”

Section: Cysteamine Modulates Reactive Oxygen Species Generationmentioning

confidence: 99%

Cysteamine Modulates Oxidative Stress and Blocks Myofibroblast Activity in CKD

Okamura

Bahrami

Ren

et al. 2014

Journal of the American Society of Nephrology

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Therapy to slow the relentless expansion of interstitial extracellular matrix that leads to renal functional decline in patients with CKD is currently lacking. Because chronic kidney injury increases tissue oxidative stress, we evaluated the antifibrotic efficacy of cysteamine bitartrate, an antioxidant therapy for patients with nephropathic cystinosis, in a mouse model of unilateral ureteral obstruction. Fresh cysteamine (600 mg/kg) was added to drinking water daily beginning on the day of surgery, and outcomes were assessed on days 7, 14, and 21 after surgery. Plasma cysteamine levels showed diurnal variation, with peak levels similar to those observed in patients with cystinosis. In cysteamine-treated mice, fibrosis severity decreased significantly at 14 and 21 days after unilateral ureteral obstruction, and renal oxidized protein levels decreased at each time point, suggesting reduced oxidative stress. Consistent with these results, treatment of cultured macrophages with cysteamine reduced cellular generation of reactive oxygen species. Furthermore, treatment with cysteamine reduced a-smooth muscle actin-positive interstitial myofibroblast proliferation and mRNA levels of extracellular matrix proteins in mice and attenuated myofibroblast differentiation and proliferation in vitro, but did not augment TGF-b signaling. In a study of renal ischemia reperfusion, cysteamine therapy initiated 10 days after injury and continued for 14 days decreased renal fibrosis by 40%. Taken together, these data suggest previously unrecognized antifibrotic actions of cysteamine via TGF-b-independent mechanisms that include oxidative stress reduction and attenuation of the myofibroblast response to kidney injury and support further investigation into the potential benefit of cysteamine therapy in the treatment of CKD.

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Comparative EPR study of different macrophage types stimulated for superoxide and nitric oxide production

Cited by 15 publications

References 42 publications

Pivotal Role of Reactive Oxygen Species in Differential Regulation of Lipopolysaccharide-Induced Prostaglandins Production in Macrophages

Pivotal Role of Reactive Oxygen Species in Differential Regulation of Lipopolysaccharide-Induced Prostaglandins Production in Macrophages

Role of oxidative stress and apoptosis in the cellular response of murine macrophages uponLeishmaniainfection

Cysteamine Modulates Oxidative Stress and Blocks Myofibroblast Activity in CKD

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