When you think about the effects of cannabis on the immune system, you might consider its ability to reduce the number of infection-fighting cells in your body. This may be because the marijuana plant interacts with CB2 receptors, which suppress inflammatory responses. As a result, your body is more susceptible to bacterial, viral, parasitic and fungal infections. For this reason, people who are undergoing chemotherapy often find that they are not able to fight infections as well as they would otherwise.
Reduces infection-fighting cells in people undergoing chemotherapy
Cancer and chemotherapy can damage your immune system. This is a serious problem, and can lead to infection. You should talk with your doctor about this risk. There are steps you can take to prevent infection and treat any that occur.
One way to lower your infection risk is to keep your hands clean. Use hand sanitizers with at least 60 percent alcohol to rub over your hands before and after you eat or go to the bathroom. It’s also a good idea to wash your hands frequently.
Another thing you can do is to avoid contact with anyone who is currently undergoing cancer treatment. They are especially at risk for infections seven to 14 days after chemo.
You should ask your oncologist for more information about precautions. If you are at a high risk for infection, your oncologist may prescribe a colony-stimulating factor. These are given as an injection or as a skin patch. Some patients experience severe side effects.
Your white blood cells are important in fighting infections. The spleen is full of these cells. Infection-fighting lymphocytes include B cells and T cells. Each type of cell has a different job. Specifically, B cells help make antibodies, which latch onto the surface of invading bacteria.
If your white blood cell count is low, you are at a higher risk for infection. Usually, the number of white blood cells returns to normal after you finish your treatment.
Suppresses inflammatory immune responses
Acute respiratory distress syndrome (ARDS) is a very serious inflammatory lung disease. It is characterized by the presence of protein rich exudates in alveolar spaces, an increased inflammatory response, and dysregulation of anti-inflammatory pathways.
The CD200/CD200R pathway has been shown to be essential for suppressing the inflammation induced by LPS. However, how CD200/CD200R modulate the inflammatory response is less understood. Consequently, further investigations are needed. In particular, the pharmacology of CD200R-related molecules may be of interest.
The discovery of a potent agonist of the CD200/CD200R pathway has implications for multitarget therapy strategies. For example, a CD200 agonist has the potential to ameliorate experimental autoimmune encephalomyelitis in SJL/J mice.
The CD200/CD200R system is also known to play a role in the regulation of the inflammatory response triggered by viral infection. Consequently, it is of interest to study the effect of this interaction on lung injury.
An interesting feature of the CD200/CD200R pathway is the ability to selectively regulate the acute inflammatory response to LPS. This is achieved through the ability of CD200 to inhibit viral replication. To investigate this, naive rats and KO rats were exposed to intratracheal LPS, and a sham vehicle was used as a control. Both groups were compared in terms of IL-6, CXCL2, and chemokines. Compared to naive rats, CD200 KO rats showed a markedly greater inflammatory response to LPS.
While the CD200/CD200R pathway is a powerful anti-inflammatory rheostat, further studies are needed to better understand its specificity.
A number of studies have been conducted over the past several years. One such study was able to find that the human body is home to several unique microbial communities. These groups have been dubbed the microbial microbiome, the mycobiome and the respiratory microbiome. Some of these microbial communities are known to play a role in the maintenance of health and to ward off disease causing agents. Other microbial communities are not so fortunate. They are often a source of infection. For example, influenza is a common affliction that can lead to significant changes in the microbial community of the human respiratory tract.
In short, the microbial world is home to several bacterial and fungal species that have become resistant to conventional antibiotics. This has led to the development of an ever increasing number of drug resistant infections. The most notable of these is Candida auris. As with many ailment related disorders, treatment is largely reliant on the patient’s clinical response.
A small sample size suggests that we are still in the dark when it comes to the true complexities of the human respiratory microbiome. It is also no surprise that the microbial world is not the only place where pathogenic germs are a concern. Thus, the most effective approach to combating these illnesses is to keep the patient on a path toward recovery, while avoiding the pitfalls associated with long stays in the hospital.
Inhibits T-cell-mediated antitumor immunity
Inhibiting T-cell-mediated antitumor immunity has become a promising new therapeutic approach for a variety of tumor entities. This research area is rapidly evolving. Various strategies are currently being investigated, including targeting CD73, a member of the B7 ligand family, which plays a central role in regulating immune regulation.
One of the first studies investigating the potential of CD73 inhibition as a therapeutic strategy was performed in breast cancer patients. Several inhibitors are under development and are being tested in early clinical trials. MEDI9447, a small molecule that inhibits the ectonucleotidase activity of CD73, has been shown to increase antitumor immunity in mice.
Another study found that CD73 upregulation is associated with poor prognosis in melanoma patients progressing under immune checkpoint blockade. The expression of CD73 is also found in cancer associated fibroblasts (CAFs), which are a key stromal component in the majority of tumor microenvironments.
CD73 has been shown to exert an adenosinergic effect, which has been extensively studied in a range of immune cell populations. The effect is thought to be related to an enhanced proliferation of dendritic cells and a reduction in the presence of tumor infiltrating lymphocytes (TILs).
Blocking the T-cell-mediated adenosinergic pathway has been demonstrated in the tumor microenvironment of irradiated tumors. Additionally, anti-CD73 treatment increases the infiltration of CD8+ T cells, which increases the overall antitumor activity of immunotherapy.
Suppresses cytokines and immune mobilization via activation of CB2 receptors
Cannabinoid inhibition of proinflammatory cytokine production is an important mechanism of immune suppression. Specifically, CB1 and CB2 receptors interact to suppress the production of IL-12, IL-6, and nitric oxide in LPS-induced inflammation. Similarly, cannabinoid receptor antagonists suppress the production of IL-12Rb2, which is essential for the innate immune response against Legionella pneumophila.
These mechanisms are involved in both the innate and adaptive phases of immunity. They include interactions with the endocrine system, as well as the neuroimmunoendocrine network. In addition, endocannabinoids are produced in the body, which inhibit inflammatory reactions. This explains why cannabinoids have anti-inflammatory effects in many inflammatory diseases, including autoimmune disorders.
The intracellular TLR7 to TLR9 pathways are known to induce type I interferon (IFN) production. Moreover, TLR2 pairs with TLR6 to stimulate cell activation through diverse pathways. For example, CD36 functions as a scavenger receptor in monocytes. When TLR2/6 is activated, TIRAP (a TIR-containing adaptor protein) and MyD88 are required for signal transduction.
CB2R stimulation suppresses viral replication and has anti-inflammatory effects in various inflammatory diseases. It also has a protective effect against the development of sepsis. Activation of CB2Rs may therefore be a useful therapeutic target in the treatment of inflammatory pathologies.
Despite the beneficial effects of cannabinoid therapy in the treatment of inflammatory diseases, it has been observed that it can lead to adverse effects. However, the mechanism of cannabinoid-induced immune suppression is not well understood. A possible mechanism involves the regulation of the p42/p44 MAPK pathway. Excessive activation of this pathway may generate a negative feedback loop.
Can be used to treat inflammatory disorders
Inflammation is an important part of the body’s immune response to pathogens. It produces chemicals that stimulate nerves and tissues, and can cause pain, swelling, and redness. However, it also can lead to organ dysfunction and tissue damage. Fortunately, there are treatments available for inflammatory disorders.
Acute inflammation can last for hours or even days, and can be triggered by a variety of factors. Some common causes include infections and mechanical injuries. The immune system responds by sending white blood cells to the area and releasing chemicals that help the body fight the infection.
Chronic inflammation is more serious, as it can cause tissue death. In order to treat chronic inflammation, there are medications that can be applied topically, as well as those that can be taken intravenously. These medications can have harsh side effects, however, and should be used with caution.
Fortunately, particle-based therapeutics can be used to modify inflammation in a targeted fashion. These particles can be designed for specific inflammatory sites and materials, and can be modified to interact with immune cells and cytokines.
Polymeric particle systems are ideal for a variety of different uses, including the treatment of inflammatory diseases. They are easily manufactured and optimized, and they provide an ideal platform for immune modulation.
Several inflammatory mouse models have shown the effectiveness of polymeric microparticles for controlling inflammatory responses. They can be customized to target specific inflammatory sites and materials, and can also be surface-modified with antibodies against leukocyte adhesion molecules.