Activation of the macrophage respiratory burst by phorbol myristate acetate: Evidence for both tyrosine-kinase-dependent and -independent pathways

Green, Simon P.; Phillips, Wayne A.

doi:10.1016/0167-4889(94)90175-9

Cited by 28 publications

(15 citation statements)

References 32 publications

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“…However, in certain cells such as murine vascular endothelial cell END-D and N9 microglial cells it was shown to augment NO production (Glozak et al, 2005;Huuskonen et al, 2004;Morikawa et al, 2004). Phorbol myristate acetate is an activator of protein kinase C which stimulates respiratory burst activities in macrophages (Green and Phillips, 1994;Rath et al, 2003). Butyrate augmented DCF-DA oxidation stimulated by PMA in contrast to its NO suppressive activity induced by stimulation with LPS.…”

Section: Discussionmentioning

confidence: 93%

Effect of butyrate on immune response of a chicken macrophage cell line

Zhou

Packialakshmi

Makkar

et al. 2014

Veterinary Immunology and Immunopathology

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Section: Discussionmentioning

confidence: 93%

Effect of butyrate on immune response of a chicken macrophage cell line

Zhou

Packialakshmi

Makkar

et al. 2014

Veterinary Immunology and Immunopathology

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“…In the lung, alveolar macrophages remove the metal ions by phagocytosis. Alveolar macrophages are the main cells involved in the first line of defense and are responsible for engulfing and eliminating any element identified as “non‐self.” A known and distinctive feature of phagocytes is their ability to respond to appropriate stimuli by activation of a respiratory burst 38, 39. The respiratory burst involves the increased production of reactive oxygen species (ROS), mainly the superoxide anion, from the reduction of oxygen by NADPH oxidase.…”

Section: Introductionmentioning

confidence: 99%

Effect of titanium dioxide on the oxidative metabolism of alveolar macrophages: An experimental study in rats

Olmedo

Tasat

Guglielmotti

et al. 2005

J Biomedical Materials Res

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Metallic implants of titanium are used therapeutically in biomedicine because of its excellent biocompatibility. However, no metal or alloy is completely inert. We have previously shown that titanium oxide (TiO(2)) is transported in blood by phagocytic monocytes and deposited in organs such as liver, spleen, and lung 6 months after intraperitoneal injection (ip). Furthermore, it is well known that exposure to metal traces alters the cellular redox status. Thus, the aim of the present study was to determine the presence of titanium in target organs after chronic exposure, assess the potential structural alterations, and evaluate the oxidative metabolism of alveolar macrophages (AM) in the lung. Rats were ip injected with 1.60 g/100 g body wt of TiO(2) in saline solution. Organs (liver, spleen, lung) were processed for histological evaluation. Reactive oxygen species (ROS) in AM obtained by bronchoalveolar lavage (BAL) were evaluated using the nitroblue tetrazolium test and quantitative evaluation by digital image analysis. The histological analysis of organs revealed the presence of titanium in the parenchyma of these organs with no associated tissue damage. Although in lung alveolar macrophages TiO(2) induced a significant rise in ROS generation, it failed to cause tissue alteration. This finding may be attributed to an adaptive response.

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“…20, 32-34 Our data depicts the importance of PMA as an oxidative burst activator at low concentration dosages, and also agrees with previous findings that PMA can deactivate macrophages upon overstimulation. 4 The dose responses reported here provide further metabolic insight into the PMA activation pathway, 35, 36 as well as the macrophage metabolic response to desensitization by PMA overexposure. In addition to increasing the understanding of the metabolic effects by PMA, this data is useful for our metabolic comparisons with clinically relevant virulence factors such as LPS and LAM.…”

Section: Discussionmentioning

confidence: 71%

“…20, 32-34 This research has afforded the knowledge that protein kinase C (PKC), which leads to NADPH oxidase complex formation and oxidative burst, can be rapidly activated by minute amounts of PMA. 35, 36 However, the actual amount of PMA needed for oxidative burst induction varies wildly in the literature from 2 nM to 20 μM, as does the exposure time from seconds to multiple hours. To better understand the macrophage metabolic response to PMA exposure, we employed the MAMP to (1) examine whether the expected response would plateau or reverse in a concentration dependent manner and to (2) compare the dose response data of known PMA pathways with those of lesser understood agents to see if any mechanistic insight could be gained.…”

Section: Resultsmentioning

confidence: 99%

Multianalyte Microphysiometry of Macrophage Responses to Phorbol Myristate Acetate, Lipopolysaccharide, and Lipoarabinomannan

et al. 2013

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This study examined the hypothesis that mycobacterial antigens generate different metabolic responses in macrophages as compared to gram-negative effectors and macrophage activators. The metabolic activation of macrophages by PMA is a useful tool for studying virulent agents and can be compared to other effectors. While phorbol myristate acetate (PMA) is commonly used to study macrophage activation, the concentration used to create this physiological response varies. The response of RAW-264.7 macrophages is concentration-dependent, where the metabolic response to high concentrations of PMA decreases suggesting deactivation. The gram-negative effector, lipopolysaccharide (LPS), was seen to promote glucose and oxygen production which were used to produce a delayed onset of oxidative burst. Pre-incubation with interferon-γ (IFN-γ) increased the effect on cell metabolism, where the synergistic effects of IFN-γ and LPS immediately initiated oxidative burst. These studies exhibited a stark contrast with lipoarabinomannan (LAM), an antigenic glycolipid component associated with the bacterial genus Mycobacterium. The presence of LAM effectively inhibits any metabolic response preventing consumption of glucose and oxygen for the promotion of oxidative burst and to ensure pathogenic proliferation. This study demonstrates for the first time the immediate inhibitory metabolic effects LAM has on macrophages, suggesting implications for future intervention studies with Mycobacterium tuberculosis.

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Activation of the macrophage respiratory burst by phorbol myristate acetate: Evidence for both tyrosine-kinase-dependent and -independent pathways

Cited by 28 publications

References 32 publications

Effect of butyrate on immune response of a chicken macrophage cell line

Effect of butyrate on immune response of a chicken macrophage cell line

Effect of titanium dioxide on the oxidative metabolism of alveolar macrophages: An experimental study in rats

Multianalyte Microphysiometry of Macrophage Responses to Phorbol Myristate Acetate, Lipopolysaccharide, and Lipoarabinomannan

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