In vivo modulation of LPS-induced alterations in brain and peripheral cytokines and HPA axis activity by cannabinoids

 In vivo modulation of LPS-induced alterations in brain and peripheral cytokines and HPA axis activity by cannabinoids},
  author={Michelle Roche and Michael Diamond and John P Kelly and David P. Finn},
  journal={Journal of Neuroimmunology},

Augmentation of endogenous cannabinoid tone modulates lipopolysaccharide‐induced alterations in circulating cytokine levels in rats

In conclusion, inhibition of endocannabinoid degradation or transport in vivo potentiates LPS‐induced increases in circulating TNF‐α levels, an effect which may be mediated by PPARγ and is also reduced by pharmacological blockade of CB1, CB2 and TRPV1.

Endocannabinergic Modulation of Interleukin-1β in Mouse Hippocampus under Basal Conditions and after in vivo Systemic Lipopolysaccharide Stimulation

CB1Rs are responsible for the modulation of basal IL-1β levels in the hippocampus, while the effects of CB1 antagonists on systemic LPS-induced IL- 1β concentrations are independent of CB 1Rs.

following Pharmacological inhibition of endocannabinoid degradation modulates the expression of inflammatory mediators in the hypothalamus following an immunological stressor

There is evidence for a role for FAAH in the regulation of LPS-induced expression of inflammatory mediators in the hypothalamus, which has fundamental physiological and potential therapeutic significance in the context of stress-related disorders.

New Insights into Cytokine Gene Expression in the Rat Hypothalamus Following Endotoxin Challenge

This is the first demonstration that prior exposure to an endotoxin can differentially affect cytokine expression in the brain and peripheral tissues when a host is confronted with a second, acute, pro-inflammatory stimulus.



Endogenous Interleukin-1 Receptor Antagonist Mediates Anti-Inflammatory and Neuroprotective Actions of Cannabinoids in Neurons and Glia

It is reported for the first time that both CB1 and CB2 receptors modulate release of endogenous IL-1ra from primary cultured glial cells, and this data suggest a novel neuroprotective mechanism of action for CBs in response to inflammatory or excitotoxic insults.

Role of cannabinoid CB1 receptors and tumor necrosis factor‐α in the gut and systemic anti‐inflammatory activity of SR 141716 (Rimonabant) in rodents

Evidence is provided that the indomethacin model of intestinal lesions differs in rat and mouse and support the existence of several mechanisms for the antiulcer activity of SR141716, the most important involving the inhibition of TNF production.

Effects of cannabinoid receptor agonist and antagonist ligands on production of inflammatory cytokines and anti-inflammatory interleukin-10 in endotoxemic mice.

Findings indicate a role for the CB1 receptor subtype in cytokine modulation by CB ligands in mice primed with Corynebacterium parvum and unprimed mice.

Cannabinoids inhibit LPS‐inducible cytokine mRNA expression in rat microglial cells

It is demonstrated that cannabinoids can modulate levels of cytokine mRNA in rat microglial cells; however, the inhibition of cytokin mRNA expression is apparently not mediated through either the CB1 or CB2 cannabinoid receptors.

The central cannabinoid receptor (CB1) mediates inhibition of nitric oxide production by rat microglial cells.

Results indicate a functional linkage between the CB1 receptor and cannabinoid-mediated inhibition of NO production by rat microglial cells.

Effect of anandamide uptake inhibition in the production of nitric oxide and in the release of cytokines in astrocyte cultures

The ability of UCM707 to reinforce the beneficial effects induced by anandamide and make it an attractive candidate for the management of those pathologies with neuroinflammation as one of their hallmarks is confirmed.

Role of circulating endotoxin and interleukin-6 in the ACTH and corticosterone response to intraperitoneal LPS.

The results suggest that circulating endotoxin is required for the activation of the HPA axis and favor a role for circulating IL-6 in this response.