Phagocytosis induces superoxide formation and apoptosis in macrophages

Park, Jae-Bong

doi:10.1038/emm.2003.44

Cited by 93 publications

(70 citation statements)

References 70 publications

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“…Conversely, RhoA was activated by the stimulation of SOZ: RhoA was translocated from cytosol to membrane, GTP-bound form of RhoA was well as both Rac1 and Rac2 was increased ( Figure 3C). Furthermore, SOZ heavily induced dorsal membrane ruffles that might enclose and engulf the particles into inside of the cells ( Figure 3D) (Park, 2003).…”

Section: Rho Is Essential For the Superoxide Formation In Macrophagesmentioning

confidence: 99%

Downstream components of RhoA required for signal pathway of superoxide formation during phagocytosis of serum opsonized zymosans in macrophages

Kim

Kim²,

Jeon³

et al. 2005

Exp Mol Med

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Rac1 and Rac2 are essential for the control of oxidative burst catalyzed by NADPH oxidase. It was also documented that Rho is associated with the superoxide burst reaction during phagocytosis of serum-(SOZ) and IgG-opsonized zymosan particles (IOZ). In this study, we attempted to reveal the signal pathway components in the superoxide formation regulated by Rho GTPase. Tat PHOX may be subsequently activated, leading to activation of NADPH oxidase to produce superoxide.

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Section: Rho Is Essential For the Superoxide Formation In Macrophagesmentioning

confidence: 99%

Downstream components of RhoA required for signal pathway of superoxide formation during phagocytosis of serum opsonized zymosans in macrophages

Kim

Kim²,

Jeon³

et al. 2005

Exp Mol Med

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“…219 This process assists in the chemical dissolution of the particle. 219 Depending on the type of receptor used in the detection of the particle, macrophages may also release intercellular chemical messengers alerting the immune system that an infection is present. 4.…”

Section: Lower Airways Clearance: Phagocytosis and Passive Uptakementioning

confidence: 99%

“…214 Lysosomes release protease ͑which break down proteins͒ and nicotinamide adenine dinucleotide phosphate ͑NADPH͒ oxidase ͑oxygen radicals͒. 219 This process assists in the chemical dissolution of the particle. 219 Depending on the type of receptor used in the detection of the particle, macrophages may also release intercellular chemical messengers alerting the immune system that an infection is present.…”

Section: Lower Airways Clearance: Phagocytosis and Passive Uptakementioning

confidence: 99%

“…After the binding of the phagocyte receptor with a ligand, the cytoskeleton ͑a network of protein filaments͒ of the phagocyte rearranges, resulting in pseudopod formation, and ultimately leading to internalization of the particle with the formation of a phagocytic vesicle ͑phagosome͒. 219 3. The phagosome fuses with a lysosome ͑an organelle containing digesting enzymes͒, forming a phagolysosome.…”

Section: Lower Airways Clearance: Phagocytosis and Passive Uptakementioning

confidence: 99%

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Nanomaterials and nanoparticles: Sources and toxicity

2007

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This review is presented as a common foundation for scientists interested in nanoparticles, their origin, activity, and biological toxicity. It is written with the goal of rationalizing and informing public health concerns related to this sometimes-strange new science of 'nano', while raising awareness of nanomaterials' toxicity among scientists and manufacturers handling them. We show that humans have always been exposed to tiny particles via dust storms, volcanic ash, and other natural processes, and that our bodily systems are well adapted to protect us from these potentially harmful intruders. The reticuloendothelial system in particular actively neutralizes and eliminates foreign matter in the body, including viruses and non-biological particles. Particles originating from human activities have existed for millennia, e.g. smoke from combustion and lint from garments, but the recent development of industry and combustion-based engine transportation has profoundly increased anthropogenic particulate pollution. Significantly, technological advancement has also changed the character of particulate pollution, increasing the proportion of nanometer-sized particles -"nanoparticles" and expanding the variety of chemical compositions. Recent epidemiological studies have shown a strong correlation between particulate air pollution levels, respiratory and cardiovascular diseases, various cancers, and mortality. Adverse effects of nanoparticles on human health depend on individual factors such as genetics and existing disease, as well as exposure, and nanoparticle chemistry, size, shape, agglomeration state, and electromagnetic properties. Animal and human studies show that inhaled nanoparticles are less efficiently removed than larger particles by the macrophage clearance mechanisms in the lung, causing lung damage, and that nanoparticles can translocate through the circulatory, lymphatic, and nervous systems to many tissues and organs, including the brain. The key to understanding the toxicity of nanoparticles is that their minute size, smaller than cells and cellular organelles, allows them to penetrate these basic biological structures, disrupting their normal function. Examples of toxic effects include tissue inflammation, and altered cellular redox balance toward oxidation, causing abnormal function or cell death. The manipulation of matter at the scale of atoms, "nanotechnology", is creating many new materials with characteristics not always easily predicted from current knowledge. Within the near-limitless diversity of these materials, some happen to be toxic to biological systems, others are relatively benign, while others confer health benefits. Some of these materials have desirable characteristics for industrial applications, as nanostructured materials often exhibit beneficial properties, from UV absorbance in sunscreen to oil-less lubrication of motors. A rational science-based approach is needed to minimize harm caused by these materials, while supporting continued study and appropriate industrial develop...

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“…Since neither phagocyte spreading nor microsphere uptake can be effectively monitored in the intact nerve, we approached this question by measuring the production of reactive oxygen species (ROS). Enhanced ROS production, also known as the 'oxidative burst', is a hallmark of phagocyte activity that can be monitored through the use of oxidation-sensitive fluorescent probes (Donko et al, 2005;Lehmann et al, 2000;Park, 2003;Sumimoto et al, 2005). In these experiments we used 5-(and-6)-chloromethyl-2Ј7Ј-dichlorodihydrofluorescein diacetate acetyl ester (CM-H 2 DCFDA), a cell-permeant indicator for ROS with enhanced intracellular retention characteristics.…”

Section: Rgd-peptides Modulate the Phagocytic Response To Nerve Injurymentioning

confidence: 99%

RGD-dependent mechanisms in the endoneurial phagocyte response and axonal regeneration in the nervous system of the snail Lymnaea stagnalis

Hermann

Nicol

Bulloch

et al. 2008

Journal of Experimental Biology

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SUMMARYActivation of phagocytic cells in the injury zone is a crucial step in the regeneration of peripheral axons. Many aspects of the mechanisms underlying the recruitment of active phagocytes remain, however, unclear. Notably, our understanding of the interactions between injury, extracellular matrix (ECM) degradation and phagocyte activation is limited. Most animal cell types, phagocytes included, interact with proteins of the ECM through one or more members of the integrin family, transmembrane cell adhesion receptors that typically bind their ligands through short linear amino acid sequences. This study focused on the role of one of the most common of such integrin recognition sequences, the Arg-Gly-Asp (RGD) motif in the recruitment and activation of endoneurial phagocytes in the injury response of the nervous system of the pond snail Lymnaea stagnalis. Like the mammalian nervous system, the Lymnaea nervous system responds to injury with recruitment and activation of endoneurial phagocytes (i.e. phagocytes residing in Lymnaeaʼs nerves), a process involving substantial changes in the morphology, motility and adhesion status of these cells. Using synthetic water-soluble RGD-peptides, we investigated the relevance of RGD-dependent mechanisms in the activation of endoneurial phagocytes and injury response of the organ-cultured nervous system of Lymnaea. Our results show that RGD-peptides modulate various aspects of phagocyte activation (i.e. spreading response, particle engulfment, oxidative burst) in vitro and in situ and significantly affect nerve regeneration in this model system. Surprisingly, while linear RGD-analogues suppressed both phagocyte activation and axonal regeneration, a circularized RGD-peptide analogue modulated these parameters in a concentration-dependent, biphasic manner. Collectively, these results emphasize the significance of RGDdependent mechanisms in the regenerative response of the Lymnaea nervous system and implicate regulation of the cellular immune response as one of the factors in this context.

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Phagocytosis induces superoxide formation and apoptosis in macrophages

Cited by 93 publications

References 70 publications

Downstream components of RhoA required for signal pathway of superoxide formation during phagocytosis of serum opsonized zymosans in macrophages

Downstream components of RhoA required for signal pathway of superoxide formation during phagocytosis of serum opsonized zymosans in macrophages

Nanomaterials and nanoparticles: Sources and toxicity

RGD-dependent mechanisms in the endoneurial phagocyte response and axonal regeneration in the nervous system of the snail Lymnaea stagnalis

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