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Inhibition by delta-9-tetrahydrocannabinol of tumor necrosis factor alpha production by mouse and human macrophages.

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Suppression by delta-9-tetrahydrocannabinol (THC) of tumor necrosis factor (TNF) production by macrophages has not been reported previously. The present study evaluated the effect in vitro of THC on soluble TNF-alpha production by cultured murine peritoneal macrophages. THC at 5 or 10 micrograms/ml

Delta 9-tetrahydrocannabinol inhibition of tumor necrosis factor-alpha: suppression of post-translational events.

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Delta 9-tetrahydrocannabinol (delta 9-THC), the major psychoactive component of marijuana, has been shown to suppress macrophage soluble cytolytic activity. The purpose of this study was to determine whether delta 9-THC inhibited this function by affecting tumor necrosis factor-alpha (TNF-alpha).

Delta-9-tetrahydrocannabinol suppresses tumor necrosis factor alpha maturation and secretion but not its transcription in mouse macrophages.

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Various in vitro studies have shown that delta-9-tetrahydrocannabinol (THC), the major psychoactive component of marijuana, has a variety of inhibitory effects on immune functions including effects on macrophages. The present studies have examined the mechanism of THC's effects on tumor necrosis

Effect of the psychoactive metabolite of marijuana, delta 9-tetrahydrocannabinol (THC), on the synthesis of tumor necrosis factor by human large granular lymphocytes.

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The natural killer cell (NK)/3polymorphonuclear neutrophil axis has recently been identified to be important in early defense against the opportunistic fungi, Candida albicans. Repression of this system is therefore likely to contribute to susceptibility to opportunistic infections. delta

Serum proteins affect the inhibition by delta-tetrahydrocannabinol of tumor necrosis factor alpha production by mouse macrophages.

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Marijuana smoke and Delta(9)-tetrahydrocannabinol promote necrotic cell death but inhibit Fas-mediated apoptosis.

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Marijuana smoke shares many components in common with tobacco smoke except for the presence of Delta(9)-tetrahydrocannabinol (Delta(9)-THC), the psychotropic compound found only in Cannibis sativa. Delta(9)-THC has been shown to potentiate smoke-induced oxidative stress and necrotic cell death. In

The major plant-derived cannabinoid Δ(9)-tetrahydrocannabinol promotes hypertrophy and macrophage infiltration in adipose tissue.

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Synthetic cannabinoid receptor agonists activate lipoprotein lipase and the formation of lipid droplets in cultured adipocytes. Here we extend this work by examining whether Δ(9)-tetrahydrocannabinol (THC), a major plant-derived cannabinoid, increases adipocyte size in vivo. Further, possibly as a

Reactive oxygen species and p38 phosphorylation regulate the protective effect of Delta9-tetrahydrocannabinol in the apoptotic response to NMDA.

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NMDA causes oxidative stress in neurons, and produces cell death involving elements of both necrosis and apoptosis. To examine the neuroprotective mechanism of Delta9-tetrahydrocannabinol (THC) in NMDA-induced death of AF5 cells, we measured reactive oxygen species (ROS) formation after exposure to

Suppression by delta-9-tetrahydrocannabinol of lipopolysaccharide-induced and intrinsic tyrosine phosphorylation and protein expression in mouse peritoneal macrophages.

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Lipopolysaccharide (LPS, 100 ng/mL)-induced tyrosine phosphorylation of four proteins (p41, p42, p77, and p82) in mouse resident peritoneal macrophages was observed using a monoclonal anti-phosphotyrosine antibody PY20 immunoblotting method. Macrophages pretreated for 3 hr with 1 microgram

Effects of delta-9-tetrahydrocannabinol administered subcutaneously to rabbits for 28 days.

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Subcutaneous (s.c.) administration of delta-9-tetrahydrocannabinol (delta-9-THC) to rabbits produced dose-related cumulative toxicity. Five groups of three New Zealand albino rabbits each received 28 daily treatments with isotonic saline, sesame oil of 15.9, 45.0 or 153.4 mg/kg/day of delta-9-THC

delta 9-Tetrahydrocannabinol, cytokines, and immunity to Legionella pneumophila.

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The major psychoactive component of marijuana, delta 9-tetrahydrocannabinol (THC), has been shown to suppress the functions of various immune cells. However, the relationship of these findings to THC-induced suppression of host resistance to infection has not been firmly established. In this report,

Delta 9-tetrahydrocannabinol injection induces cytokine-mediated mortality of mice infected with Legionella pneumophila.

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Delta 9-Tetrahydrocannabinol (THC) injection modulates immune cell function, but the significance of this in altering host resistance to infection is not understood. In addition, exposure to THC and other drugs of abuse during infection is associated with an acute mortality syndrome. We examined the

Cannabinoid receptor CB2 is involved in tetrahydrocannabinol-induced anti-inflammation against lipopolysaccharide in MG-63 cells.

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Cannabinoid Δ9-tetrahydrocannabinol (THC) is effective in treating osteoarthritis (OA), and the mechanism, however, is still elusive. Activation of cannabinoid receptor CB2 reduces inflammation; whether the activation CB2 is involved in THC-induced therapeutic action for OA is still unknown.

Selective inhibition of natural killer but not natural cytotoxic activity in a cloned cell line by delta-9-tetrahydrocannabinol.

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Natural killer (NK) and natural cytotoxic (NC) activities are spontaneously generated against certain tumors in vitro and their contribution to tumor immunity is being extensively investigated. We report here that the interleukin-2 (IL-2)-dependent murine cell line, NKB61A2, which we recently found

delta 9-Tetrahydrocannabinol (THC) modulates IL-1 bioactivity in human monocyte/macrophage cell lines.

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We have previously observed that delta 9-tetrahydrocannabinol (THC), the major psychoactive component of marijuana, increased supernatant interleukin-1 (IL-1) bioactivity in cultures of mouse resident peritoneal macrophages stimulated with lipopolysaccharide (LPS). In this study, experiments were

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