Differential expression of the CB2 cannabinoid receptor by rodent macrophages and macrophage-like cells in relation to cell activation

Carlisle, Steven J.; Marciano‐Cabral, Francine; Staab, A; Ludwick, Christina; Cabral, Guy A.

doi:10.1016/s1567-5769(01)00147-3

Cited by 314 publications

(295 citation statements)

References 29 publications

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“…Mouse peritoneal macrophages and rodent macrophage cell lines express CB 2 receptor mRNA, and this message is more abundant than the message for CB 1 (Carlisle et al, 2002). Rat peritoneal macrophages also express CB 2 receptors (Carlisle et al, 2002). In peripheral macrophages, like in their CNS counterpart, CB 2 receptor expression may be modulated by the activation state of the cell.…”

Section: Peripheral Immune Cells Express Cannabinoid Receptorsmentioning

confidence: 99%

“…Primary cultures of rat and mouse microglia express both CB 1 and CB 2 receptor mRNA and protein (Sinha et al, 1998;Carlisle et al, 2002;Facchinetti et al, 2003;Walter et al, 2003a). Human microglia also express CB 2 receptor mRNA (Klegeris et al, 2003).…”

Section: Glial Cells Express Cannabinoid Receptorsmentioning

confidence: 99%

“…Primary mouse microglia express CB 2 receptors at the leading edges of lamellipodia and microspikes (Walter et al, 2003a), suggesting a function in motility, discussed below. The proinflammatory cytokine interferongamma (IFN-g), which is produced by T H 1 T cells and natural killer (NK) cells in MS and EAE (reviewed in Popko et al, 1997), increases CB 2 receptor mRNA and protein in rat microglia (Carlisle et al, 2002).…”

Section: Glial Cells Express Cannabinoid Receptorsmentioning

confidence: 99%

“…While it is known that cannabinoid receptor expression is modulated by cytokines in microglial cells (Carlisle et al, 2002), it is not yet known if cannabinoid receptor expression is modulated in astrocytes or oligodendrocytes. …”

Section: Glial Cells Express Cannabinoid Receptorsmentioning

confidence: 99%

“…CB 1 and CB 2 receptors are expressed by human peripheral blood cell-derived dendritic cells (DCs) (Matias et al, 2002), and mRNA for both CB 1 and CB 2 receptors is expressed in mouse bone marrow-derived DC (Klein et al, 2003). Mouse peritoneal macrophages and rodent macrophage cell lines express CB 2 receptor mRNA, and this message is more abundant than the message for CB 1 (Carlisle et al, 2002). Rat peritoneal macrophages also express CB 2 receptors (Carlisle et al, 2002).…”

Section: Peripheral Immune Cells Express Cannabinoid Receptorsmentioning

confidence: 99%

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Cannabinoids and neuroinflammation

Walter

Stella

2004

British J Pharmacology

303

215

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Growing evidence suggests that a major physiological function of the cannabinoid signaling system is to modulate neuroinflammation. This review discusses the anti-inflammatory properties of cannabinoid compounds at molecular, cellular and whole animal levels, first by examining the evidence for anti-inflammatory effects of cannabinoids obtained using in vivo animal models of clinical neuroinflammatory conditions, specifically rodent models of multiple sclerosis, and second by describing the endogenous cannabinoid (endocannabinoid) system components in immune cells. Our aim is to identify immune functions modulated by cannabinoids that could account for their antiinflammatory effects in these animal models.

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Section: Peripheral Immune Cells Express Cannabinoid Receptorsmentioning

confidence: 99%

Section: Glial Cells Express Cannabinoid Receptorsmentioning

confidence: 99%

Section: Glial Cells Express Cannabinoid Receptorsmentioning

confidence: 99%

Section: Glial Cells Express Cannabinoid Receptorsmentioning

confidence: 99%

Section: Peripheral Immune Cells Express Cannabinoid Receptorsmentioning

confidence: 99%

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Cannabinoids and neuroinflammation

Walter

Stella

2004

British J Pharmacology

303

215

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Cannabinoid signaling in glial cells

Stella

2004

Glia

201

165

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The cannabinoid signaling system is composed of cannabinoid (CB) receptors, their endogenous ligands, the endocannabinoids, and the enzymes that produce and inactivate them. It is well known that neurons communicate between each other through this signaling system. Delta 9-tetrahydrocannabinol, the main psychoactive compound of marijuana, interacts with CB receptors, impinging on this communication and inducing profound behavioral effects such as memory impairment and analgesia. Recent evidence suggests that glial cells also express components of the cannabinoid signaling system and marijuana-derived compounds act at CB receptors expressed by glial cells, affecting their functions. This review summarizes this evidence, discusses how glial cells might use the cannabinoid signaling system to communicate with neighboring cells, and argues that nonpsychotropic cannabinoids, both marijuana-derived and synthetic, likely constitute lead compounds for therapy aimed at reducing acute and chronic neuroinflammation, such as occurs in multiple sclerosis.

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Synthetic cannabinoid WIN55,212‐2 inhibits generation of inflammatory mediators by IL‐1β‐stimulated human astrocytes

Sheng

Min

et al. 2004

Glia

220

178

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Activated glial cells have been implicated in the neuropathogenesis of many infectious and inflammatory diseases of the brain. A number of inflammatory mediators have been proposed to play a role in glial cell-related brain damage; e.g., free radicals such as nitric oxide (NO), cytokines, and chemokines. Our laboratory has been interested in the effect of psychoactive drugs and their derivatives on the production of these mediators. Cannabinoids have been shown to possess immunomodulatory as well as psychoactive properties. We previously have shown that interleukin (IL)-1beta-stimulated human astrocytes, but not microglia, produce NO. In this study, we investigated the effects of the synthetic cannabinoid WIN55,212-2 on the production of several key inflammatory mediators by human fetal astrocytes activated by IL-1beta. Expression of the cannabinoid receptors CB1 and CB2 was detected on human astrocytes. WIN55,212-2 (10(-5) M) potently inhibited inducible NO synthase (iNOS) and corresponding NO production by IL-1beta-stimulated astrocytes. The CB1 and CB2 receptor-specific antagonists SR141716A and SR144528, respectively, partially blocked this suppressive effect. In addition, treatment of astrocytes with WIN55,212-2 downregulated in a concentration-dependent manner IL-1beta-induced tumor necrosis factor (TNF)-alpha release. Treatment with WIN55,212-2 also inhibited production of the chemokines CXCL10, CCL2 and CCL5 by IL-1beta-activated astrocytes. These findings indicate that WIN55,212-2 inhibits the production of inflammatory mediators by IL-1beta-stimulated human astrocytes and suggest that comparable agents may have therapeutic potential for the management of brain inflammation.

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Differential expression of the CB2 cannabinoid receptor by rodent macrophages and macrophage-like cells in relation to cell activation

Cited by 314 publications

References 29 publications

Cannabinoids and neuroinflammation

Cannabinoids and neuroinflammation

Cannabinoid signaling in glial cells

Synthetic cannabinoid WIN55,212‐2 inhibits generation of inflammatory mediators by IL‐1β‐stimulated human astrocytes

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