Access to medical and recreational marijuana has been growing in the United States, and its increased interest has raised the question of how cannabis interacts with the human body beyond recreational or medicinal uses such as pain management. Although cannabis has anti-inflammatory properties, it can also lead to allergic reactions in some people.
“There is still so much we don’t know about this plant and how the human body responds to it,” says Thomas Jefferson University pulmonary researcher Ajay Nayak, PhD.
With over 11,000 cannabis strains in circulation, each with unique chemical profiles, understanding the intricate interactions between these strains and the human body remains a significant challenge.
“For something that’s becoming increasingly accessible, we should understand its benefits and acknowledge the context in which certain components could be harmful,” says Dr. Nayak.
A handful of studies have shown that using cannabis or being in an environment around the plant, such as in a processing facility, can lead to breathing problems, exacerbate asthma and cause hives and swelling. With more and more states legalizing marijuana, Dr. Nayak anticipates that more people are at risk for allergic reactions. “This is an emerging public health issue,” he says.
Dr. Nayak and his colleagues in the department of medicine, Cali Loblundo and Leonard Bielory, recently published an article in The Journal of Allergy and Clinical Immunology that reviews the current research surrounding immune responses to cannabis. The authors discuss the likely culprits of an allergic reaction to cannabis, which surprisingly do not include THC (tetrahydrocannabinol, the principal psychoactive compound) and the immune reactions that appear most commonly.
“Our aim is to educate physicians because we rely on them to educate patients,” Dr. Nayak says. “As cannabis use increases, we need to think about whether physicians have the essential knowledge to navigate through this change.” Dr. Nayak is working to develop diagnostic tools to test for cannabis allergy.
By Roni Dengler
People living with HIV infection for a decade or more can experience neurological symptoms, including cognitive deficits. However, whether the cognitive issues are caused by the virus, years of antiviral medicines or normal aging — or some combination thereof — has been difficult to ascertain. A new study by Thomas Jefferson University researchers has identified a molecular mechanism that HIV has on small blood vessels in the brain that appears to accelerate changes that often occur with age.
The researchers focused on a protein produced by the virus, called Tat (Trans-Activator of Transcription), testing it in cell culture and in mice — and looking for it in postmortem brains from people with HIV-associated neurocognitive disease. Their findings show that Tat causes oxidative stress in the cells lining blood vessels that leads to a thickening of the vessel walls. This thickening can result in mini-stroke type activity, which starves surrounding cells of oxygen — including neurons. Hypoxia, in turn, increases mitochondrial activity within cells, creating more oxidative stress in a kind of vicious cycle.
“This is one part of the picture,” says Jarin Hongpaisan, DVM, PhD, an assistant professor of medicine who studies the molecular biology of neurodegeneration. “The neurodegenerative disease is a combination of many things, many HIV-induced changes in brain.” Dr. Hongpaisan collaborated with associate professor Mudit Tyagi, PhD, who specializes in HIV disease processes, to methodically work out the molecular pathway that directly links an HIV protein to changes in cell function, including increased oxidative stress, and reduced growth factors. The result — this one part of the picture — gives rise to changes in the small blood vessels in the brain which are similar to those seen in aging, Alzheimer’s disease and cerebrovascular disease.
By Jill U. Adams
Common sports injuries such as a torn rotator cuff, require surgery to repair. Much of the time, surgery is successful. However, for some people the repaired joint becomes very stiff and painful because scar tissue has built up in and around it. There are no treatments for this condition, known as arthrofibrosis, other than aggressive physical therapy or additional surgery.
Recently, orthopedic researchers Andrzej Fertala, PhD, and colleagues, have discovered a key difference between those who develop joint stiffness after surgery and those who do not. The discovery could potentially identify patients who would benefit from anti-scarring treatment following surgery.
To figure out who might develop arthrofibrosis following surgery, Dr. Fertala worked with the Rothman Institute orthopedic surgeons to collect tissue samples from participants undergoing surgery to repair torn rotator cuffs. The researchers also kept track of which patients returned for physical therapy or additional surgery to treat shoulder stiffness developed after surgery.
When the researchers treated cells from the tissue samples with a molecule to simulate the fibrotic healing process, they saw that levels of an enzyme called prolyl-4-hydroxylase (P4H) only increased in patients who developed stiff shoulders. They reported their results in the journal Health Science Reports.
One of P4H’s many functions in the cell is to modify protein known as procollagen I. This chemical modification ensures that procollagen I is stable and has the appropriate characteristics to heal injury. Too much of this protein however leads to excessive scar tissue and very stiff joints.
“Now, we can test for P4H, to distinguish which patients may develop joint stiffness and hence will be good candidates for pre-treatment with the anti-scarring antibody therapy that we are developing,” says Dr. Fertala.
By Roni Dengler
