Adenosine triphosphate inhibits cytokine release from lipopolysaccharide-activated microglia via P2y receptors

Ogata, Tadanori; Chuai, Miao; Morino, Tadao; Yamamoto, Haruyasu; Nakamura, Yoichi; Schubert, Peter

doi:10.1016/s0006-8993(03)03028-2

Cited by 48 publications

(52 citation statements)

References 41 publications

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“…The activation of P2Y receptors can also affect microglial secretion of cytokines and other biologically active substances. The P2Y receptors, for example, were shown to inhibit release of TNF-␣, IL-1␤, IL-6, and IL-12 in LPSactivated cultured rat and mice microglia (82,669). In contrast, the activation of P2Y 1 /P2Y 11 receptors increased IL-10 expression and release in LPS-activated rat microglia (820,821).…”

Section: P2y Receptorsmentioning

confidence: 99%

Physiology of Microglia

Kettenmann

Hanisch

Нода

et al. 2011

Physiological Reviews

3,090

2,981

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Microglial cells are the resident macrophages in the central nervous system. These cells of mesodermal/mesenchymal origin migrate into all regions of the central nervous system, disseminate through the brain parenchyma, and acquire a specific ramified morphological phenotype termed “resting microglia.” Recent studies indicate that even in the normal brain, microglia have highly motile processes by which they scan their territorial domains. By a large number of signaling pathways they can communicate with macroglial cells and neurons and with cells of the immune system. Likewise, microglial cells express receptors classically described for brain-specific communication such as neurotransmitter receptors and those first discovered as immune cell-specific such as for cytokines. Microglial cells are considered the most susceptible sensors of brain pathology. Upon any detection of signs for brain lesions or nervous system dysfunction, microglial cells undergo a complex, multistage activation process that converts them into the “activated microglial cell.” This cell form has the capacity to release a large number of substances that can act detrimental or beneficial for the surrounding cells. Activated microglial cells can migrate to the site of injury, proliferate, and phagocytose cells and cellular compartments.

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Section: P2y Receptorsmentioning

confidence: 99%

Physiology of Microglia

Kettenmann

Hanisch

Нода

et al. 2011

Physiological Reviews

3,090

2,981

View full text Add to dashboard Cite

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“…Activated microglia can also act as scavenger cells that induce apoptosis in damaged neurons by releasing toxic factors, including NO (Sanz and Di Virgilio, 2000;Inoue, 2002). Thus, whereas microglia may play an important role against infection in the CNS, overstimulation of this immune reaction may accelerate the neuronal damage caused by ischemia, trauma, or neurodegenerative dis-eases such as Alzheimer's and Parkinson's disease, human immunodeficiency virus encephalopathy, multiple sclerosis, and amyotrophic lateral scoliosis, which exhibit microglial proliferation and activation (Ogata et al, 2003). These authors showed that ATP inhibits cytokine release from lipopolysaccharide-activated microglia via P2Y receptors and suggested that P2Y agonists may be a potential treatment for toxic immunoreactions.…”

Section: A Neuroprotectionmentioning

confidence: 99%

Pathophysiology and Therapeutic Potential of Purinergic Signaling

2006

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“…ATP is a major factor mediating intercellular communication in the immune and nervous systems, and recent studies have shown that microglia possess purinigenic receptors (268,362), whose stimulation markedly affects a number of microglial cell functions, such as chemotaxis and cytokine production, that are involved in defense as well as brain damage (165). Since ATP is considered to be the dominant extracellular messenger for astrocyte-to-astrocyte communication, it has been proposed that ATP may also serve a similar function in astrocyte-to-microglial cell communication (362).…”

Section: Activated Microgliamentioning

confidence: 99%

Role of Microglia in Central Nervous System Infections

et al. 2004

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The nature of microglia fascinated many prominent researchers in the 19th and early 20th centuries, and in a classic treatise in 1932, Pio del Rio-Hortega formulated a number of concepts regarding the function of these resident macrophages of the brain parenchyma that remain relevant to this day. However, a renaissance of interest in microglia occurred toward the end of the 20th century, fueled by the recognition of their role in neuropathogenesis of infectious agents, such as human immunodeficiency virus type 1, and by what appears to be their participation in other neurodegenerative and neuroinflammatory disorders. During the same period, insights into the physiological and pathological properties of microglia were gained from in vivo and in vitro studies of neurotropic viruses, bacteria, fungi, parasites, and prions, which are reviewed in this article. New concepts that have emerged from these studies include the importance of cytokines and chemokines produced by activated microglia in neurodegenerative and neuroprotective processes and the elegant but astonishingly complex interactions between microglia, astrocytes, lymphocytes, and neurons that underlie these processes. It is proposed that an enhanced understanding of microglia will yield improved therapies of central nervous system infections, since such therapies are, by and large, sorely needed

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Adenosine triphosphate inhibits cytokine release from lipopolysaccharide-activated microglia via P2y receptors

Cited by 48 publications

References 41 publications

Physiology of Microglia

Physiology of Microglia

Pathophysiology and Therapeutic Potential of Purinergic Signaling

Role of Microglia in Central Nervous System Infections

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