​​​​​​​​cannabis data.org

Cannabis -vs- Asthma

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2828614:  Allergic asthma is a complex inflammatory disorder characterized by airway hyper-responsiveness, elevated serum IgE, recruitment of eosinophils into the lung and mucus hypersecretion by goblet cells [111]. Murine models of allergic airway disease, employing ovalbumin (OVA) as an aeroallergen, indicated that CD4+ Th2 cells (IL-4, IL-5 and IL-13) played a pivotal role in the pathophysiology of the allergic airway response [112]. Intraperitoneal administration of THC or cannabinol (CBN) in OVA-sensitized and challenged A/J mice led to attenuation of serum IgE, IL-2, IL-4, IL-5 and IL-13 mRNA expression and decreased allergen-induced mucus production, indicating that cannabinoid-based compounds may represent a novel class of therapeutic agents for the treatment of allergic airway diseases [113]. While most studies have shown that cannabinoids, such as THC, facilitate a Th1 to Th2 cytokine switch, as discussed previously, it is surprising that cannabinoids can also suppress allergic asthma triggered primarily by Th2 cytokines. It is possible that THC may affect other cells such as DCs and B cells directly in this model. Previous findings indicated that aerosolized THC was capable of causing significant bronchodilatation with minimal systemic side effects, but had a local irritating effect on the airways [114]. Further bronchodilator effects of cannabinoids administered orally or by aerosol to asthmatic patients have also been reported [115,116]. Similarly, endogenous cannabinoids have been shown to regulate airway responsiveness. In rodent lungs, a Ca2+-activated mechanism for the biosynthesis of anandamide was observed and CB1 receptors were found predominantly on axon terminals of airway nerves, indicating that endocannabinoids may regulate bronchial smooth muscle tone [117]. It was reported that activation of CB1 receptors by locally released anandamide may participate in the control of bronchial contractility. Blocking of AEA-induced CB1 activity can enhance capsaicin-induced bronchospasm. However, the authors further suggested that the effects of AEA may depend on the state of the bronchial muscle. During capsaicin-evoked bronchospasm, AEA may reduce the muscle contraction, whereas AEA may cause bronchoconstriction in the absence of vagus nerve-constricting tone [117].