Cannabinoids Decrease the Th17 Infla... [J Neuroimmune Pharmacol. 2013] - PubMed - NCBI

Marijuana's cannabinoids improve human health by reducing systemic inflammation which is a root cause for many degenerative diseases. J Neuroimmune Pharmacol. 2013 Jul 28. [Epub ahead of print]

Cannabinoids Decrease the Th17 Inflammatory Autoimmune Phenotype.

Kozela E, Juknat A, Kaushansky N, Rimmerman N, Ben-Nun A, Vogel Z.


The Dr Miriam and Sheldon G. Adelson Center for the Biology of Addictive Diseases, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel,


Cannabinoids, the Cannabis constituents, are known to possess anti-inflammatory properties but the mechanisms involved are not understood. Here we show that the main psychoactive cannabinoid, Δ-9-tetrahydrocannabinol (THC), and the main nonpsychoactive cannabinoid, cannabidiol (CBD), markedly reduce the Th17 phenotype which is known to be increased in inflammatory autoimmune pathologies such as Multiple Sclerosis. We found that reactivation by MOG35-55 of MOG35-55-specific encephalitogenic T cells (cells that induce Experimental Autoimmune Encephalitis when injected to mice) in the presence of spleen derived antigen presenting cells led to a large increase in IL-17 production and secretion. In addition, we found that the cannabinoids CBD and THC dose-dependently (at 0.1-5 μM) suppressed the production and secretion of this cytokine. Moreover, the mRNA and protein of IL-6, a key factor in Th17 induction, were also decreased. Pretreatment with CBD also resulted in increased levels of the anti-inflammatory cytokine IL-10. Interestingly, CBD and THC did not affect the levels of TNFα and IFNγ. The downregulation of IL-17 secretion by these cannabinoids does not seem to involve the CB1, CB2, PPARγ, 5-HT1A or TRPV1 receptors. In conclusion, the results show a unique cannabinoid modulation of the autoimmune cytokine milieu combining suppression of the pathogenic IL-17 and IL-6 cytokines along with boosting the expression of the anti-inflammatory cytokine IL-10.

via Cannabinoids Decrease the Th17 Infla... [J Neuroimmune Pharmacol. 2013] - PubMed - NCBI.

Promotion of β-amyloid production by C-reactiv... [Neurochem Int. 2012] - PubMed - NCBI

The inflammatory compound, C-reactive protein, is involved in the development of Alzheimer's disease, other forms of dementia, heart disease, diabetes and most likely cancer and arthritis. A solid study of a large population sample found that people who smoked marijuana at least three times per week had half of the blood levels of C-reactive protein as those who did not use marijuana (Decreased prevalence of diabetes in marijuana users, 2012). This is more evidence that responsible marijuana use benefits human health by preventing disease-friendly internal environments,  interrupting disease processes. and triggering repair mechanisms. Neurochem Int. 2012 Feb                                                       Promotion of β-amyloid production by C-reactive protein and its implications in the early pathogenesis of Alzheimer's disease.         Bi BT, Lin HB, Cheng YF, Zhou H, Lin T, Zhang MZ, Li TJ, Xu JP.SourceDepartment of Pharmacology, School of Pharmaceutical Sciences, Southern Medical University, Guangzhou, Guangdong 510515, China.                                                                         Abstract: C-reactive protein CRP and β-amyloid protein Aβ are involved in the development of Alzheimer's disease AD. However, the relationship between CRP and Aβ production is unclear. In vitro and in vivo experiments were performed to investigate the association of CRP with Aβ production. Using the rat adrenal pheochromocytoma cell line PC12 cells to mimic neurons, cytotoxicity was evaluated by cell viability and supernatant lactate dehydrogenase LDH activity. The levels of amyloid precursor protein APP, beta-site APP cleaving enzyme BACE-1, and presenilins PS-1 and PS-2 were investigated using real-time polymerase chain reaction and Western blotting analysis. Aβ1-42 was measured by enzyme-linked immunosorbent assay. The relevance of CRP and Aβ as well as potential mechanisms were studied using APP/PS1 transgenic Tg mice. Treatment with 0.5-4.0 μM CRP for 48 h decreased cell viability and increased LDH leakage in PC12 cells. Incubation with CRP at a sub-toxic concentration of 0.2 μM increased the mRNA levels of APP, BACE-1, PS-1, and PS-2, as well as Aβ1-42 production. CRP inhibitor reversed the CRP-induced upregulations of the mRNA levels of APP, BACE-1, PS-1, and PS-2, and the protein levels of APP, BACE-1, PS-1, and Aβ1-42, but did not reversed Aβ1-42 cytotoxicity. The cerebral levels of CRP and Aβ1-42 in APP/PS1 Tg mice were positively correlated, accompanied with the elevated mRNA expressions of serum amyloid P component SAP, complement component 1q C1q, and tumor necrosis factor-α TNF-α. These results suggest that CRP cytotoxicity is associated with Aβ formation and Aβ-related markers expressions; CRP and Aβ were relevant in early-stage AD; CRP may be an important trigger in AD pathogenesis.

via Promotion of β-amyloid production by C-reactiv... [Neurochem Int. 2012] - PubMed - NCBI.

Low dose oral cannabinoid therapy reduces progression... [Nature. 2005] - PubMed - NCBI

It looks like regularly ingesting small amounts of THC can protect us from developing atherosclerosis, heart disease, by reducing inflammation. As more and more research is conducted on a broad range of illnesses, it is becoming more and more apparent that cannabinoids such as THC and CBD work as health modulating tonics for our bodies--reducing inflammation, decreasing levels of harmful chemicals that wreck destruction at the cellular and genetic levels and shielding cells from damaging influences from outside of the body. It really seems that almost everyone could benefit from taking a few drops of cannabis extract in the form of a tincture just before bedtime. It is stunning that these compounds have healing effects on everything from diabetes to heart disease to cancer to depression. Prohibition harms us all by making these health-building products unavailable to the general public and by ruining lives to maintain this fraudulent cruelty. Nature. 2005 Apr 7;4347034:782-6.

Low dose oral cannabinoid therapy reduces progression of atherosclerosis in mice.

Steffens S, et al.

Abstract: Atherosclerosis is a chronic inflammatory disease, and is the primary cause of heart disease and stroke in Western countries. Derivatives of cannabinoids such as delta-9-tetrahydrocannabinol THC modulate immune functions and therefore have potential for the treatment of inflammatory diseases. We investigated the effects of THC in a murine model of established atherosclerosis. Oral administration of THC 1 mg kg-1 per day resulted in significant inhibition of disease progression. This effective dose is lower than the dose usually associated with psychotropic effects of THC. Furthermore, we detected the CB2 receptor the main cannabinoid receptor expressed on immune cells in both human and mouse atherosclerotic plaques. Lymphoid cells isolated from THC-treated mice showed diminished proliferation capacity and decreased interferon-gamma secretion. Macrophage chemotaxis, which is a crucial step for the development of atherosclerosis, was also inhibited in vitro by THC. All these effects were completely blocked by a specific CB2 receptor antagonist. Our data demonstrate that oral treatment with a low dose of THC inhibits atherosclerosis progression in the apolipoprotein E knockout mouse model, through pleiotropic immunomodulatory effects on lymphoid and myeloid cells. Thus, THC or cannabinoids with activity at the CB2 receptor may be valuable targets for treating atherosclerosis.

via Low dose oral cannabinoid therapy reduces progression... [Nature. 2005] - PubMed - NCBI.