| |
Marijuana Reduced Neuro-Inflammation in
vitro/new study/POT good or bad for you?????
| | | | |
Download the PDF here
Marijuana use impacts midlife cardiovascular events in HIV-infected men - (05/17/17)
http://www.natap.org/2017/CROI/croi_155.htm .....Cognitive Complaints and Development of Falls among HIV-Infected and Uninfected Women
"cannabis-related stroke is not a myth" new literature, authors
conclude.....http://www.natap.org/2013/newsUpdates/012413_01.htm
One Quarter of HIV+ Smoker Group Has COPD--Risk Lower With Higher CD4s.....http://www.natap.org/2014/CROI/croi_99.htm
Is cannabis use psychotogenic?.....http://www.natap.org/2006/HIV/012506_01.htm
Adverse health effects of non-medical cannabis use......http://www.natap.org/2009/HIV/101709_01.htm
Daily Cannabis Use by HCV+ Increased Odds of Moderate to Severe Fibrosis by 7- Fold.....http://www.natap.org/2006/AASLD/AASLD_07.htm
Influence of Cannabis Use on Severity of Hepatitis C Disease.....http://www.natap.org/2008/HCV/012908_01.htm ......"....In summary, we found that daily cannabis use was significantly associated with the presence of moderate to severe fibrosis compared with mild fibrosis in persons with chronic HCV infection. Furthermore, daily cannabis use and moderate to heavy alcohol use appeared to have at least multiplicative effects on the odds of severe fibrosis. On the basis of our results, we would advise that individuals with chronic HCV infection be counseled to reduce or abstain from cannabis use....daily cannabis users having nearly 7-fold higher odds of moderate to severe fibrosis compared with non-daily users. HCV-HIV coinfected subjects were significantly more likely to use cannabis daily and to have a prescription for medical cannabis than HCV monoinfected subjects. The recommendation to avoid cannabis use might be especially important for HCV-HIV coinfected persons, given that fibrosis progression is already enhanced in this group
Daily Cannabis Smoking as a Risk Factor for Fibrosis Progression in Chronic Hepatitis C.....http://www.natap.org/2005/HCV/062705_01.htm
(Marijuana/Hash) Endocannabinoids and liver disease -
review.....http://www.natap.org/2005/HCV/091905_01.htm
Tobacco and Marijuana Tied to Lower Atazanavir
Concentrations.....http://www.natap.org/2009/ICCAC/ICCAC_04.htm
The Effect of Smoked Marijuana on Chronic Neuropathic and Experimentally Induced Pain in HIV Neuropathy: Results of an Open-label Pilot Study.....http://www.natap.org/2004/CROI/croi_38.htm
----------------------------------
Public Release: 12-Dec-2017
Marijuana may help HIV patients keep mental stamina longer
Michigan State University
https://www.eurekalert.org/pub_releases/2017-12/msu-mmh121217.php
EAST LANSING, Mich. -- A chemical found in marijuana, known as tetrahydrocannabinol, or THC, has been found to potentially slow the process in which mental decline can occur in up to 50 percent of HIV patients, says a new Michigan State University study.
"It's believed that cognitive function decreases in many of those with HIV partly due to chronic inflammation that occurs in the brain," said Norbert Kaminski, lead author of the study, now published in the journal AIDS. "This happens because the immune system is constantly being stimulated to fight off disease."
Kaminski and his co-author, Mike Rizzo, a graduate student in toxicology, discovered that the compounds in marijuana were able to act as anti-inflammatory agents, reducing the number of inflammatory white blood cells, called monocytes, and decreasing the proteins they release in the body.
"This decrease of cells could slow down, or maybe even stop, the inflammatory process, potentially helping patients maintain their cognitive function longer," Rizzo said.
The two researchers took blood samples from 40 HIV patients who reported whether or not they used marijuana. Then, they isolated the white blood cells from each donor and studied inflammatory cell levels and the effect marijuana had on the cells.
"The patients who didn't smoke marijuana had a very high level of inflammatory cells compared to those who did use," Kaminski said. "In fact, those who used marijuana had levels pretty close to a healthy person not infected with HIV."
Kaminski, director of MSU's Institute for Integrative Toxicology, has studied the effects of marijuana on the immune system since 1990. His lab was the first to identify the proteins that can bind marijuana compounds on the surface of immune cells. Up until then, it was unclear how these compounds, also known as cannabinoids, affected the immune system.
HIV, which stands for human immunodeficiency virus, infects and can destroy or change the functions of immune cells that defend the body. With antiretroviral therapy - a standard form of treatment that includes a cocktail of drugs to ward off the virus - these cells have a better chance of staying intact.
Yet, even with this therapy, certain white blood cells can still be overly stimulated and eventually become inflammatory.
"We'll continue investigating these cells and how they interact and cause inflammation specifically in the brain," Rizzo said. "What we learn from this could also have implications to other brain-related diseases like Alzheimer's and Parkinson's since the same inflammatory cells have been found to be involved."
Knowing more about this interaction could ultimately lead to new therapeutic agents that could help HIV patients specifically maintain their mental function.
"It might not be people smoking marijuana," Kaminski said. "It might be people taking a pill that has some of the key compounds found in the marijuana plant that could help."
-------------------------------------------
"The results from this study show that in vitro THC treatment promotes anti-inflammatory effects on monocyte processes that are implicated in HIV-associated neuroinflammation, including monocyte transition into the CD16+ phenotype and secretion of IP-10. With these findings it is tempting to speculate that THC is one of the major components of cannabis that elicits the decrease in circulating CD16+ monocytes and serum IP-10 that was observed in HIV+MJ+ donors. However, the in vivo effects of THC when inhaled through cannabis use may be different than that observed in vitro due to the additional 60-plus cannabinoids that are present in cannabis as well as other plant-derived constituents [54]. Therefore cannabinoids in combination with other plant-associated compounds may contribute to the observed anti-inflammatory actions. In addition, cannabis use could indirectly have anti-inflammatory actions, such as through stress reduction, which can have an impact on inflammation [55, 56]"
----------------------
HIV-infected cannabis users have lower circulating CD16+ monocytes and IP-10 levels compared to non-using HIV patients
Rizzo Michael D.; Crawford, Robert B.; Henriquez, Joseph E.; Aldhamen, Yasser; Gulick, Peter; Amalfitano, Andrea; Kaminski, Norbert E.
AIDS: Nov 30 2017
Objective:
Chronic immune activation and elevated numbers of circulating activated monocytes (CD16+) are implicated in HIV-associated neuroinflammation. The objective was to compare the level of circulating CD16+ monocytes and interferon-γ-inducible protein 10 (IP-10) between HIV-infected cannabis users (HIV+MJ+) and non-cannabis users (HIV+MJ-), and determine whether in vitro Δ9-Tetrahydrocannabinol (THC), a constituent of cannabis, affected CD16 expression as well as IP-10 production by monocytes.
Design:
The levels of circulating CD16+ monocytes and IP-10 from HIV+MJ- and HIV+MJ+ donors were examined. In vitro experimentation using THC was performed on primary leukocytes isolated from HIV-MJ-, HIV+MJ- and HIV+MJ+ donors to determine if THC has an impact on CD16+ monocyte and IP-10 levels.
Methods:
Flow cytometry was used to measure the number of blood CD16+ monocytes and serum IP-10 from HIV+MJ- and HIV+MJ+ donors. Peripheral blood mononuclear cells (PBMC) were isolated from HIV-MJ- and HIV+ (MJ- and MJ+) donors for in vitro THC and IFNα treatment, and CD16+ monocytes and supernatant IP-10 were quantified.
Results:
HIV+MJ+ donors possessed a lower level of circulating CD16+ monocytes and serum IP-10, compared to HIV+MJ- donors. Further, monocytes from HIV+MJ+ donors were unable to induce CD16 expression when treated with in vitro IFNα, while HIV-MJ- and HIV+MJ- donors displayed pronounced CD16 induction, suggesting anti-inflammatory effects by cannabis. Lastly, in vitro THC treatment impaired CD16− monocyte transition to CD16+ and monocyte-derived IP-10.
Conclusions:
Components of cannabis, including THC, may decelerate peripheral monocyte processes that are implicated in HIV-associated neuroinflammation.
|
| | | | | | |
|
