Are resistant to allergen-induced inflammatory reactions. Administering a CB2 agonist inside the subsequent component with the experiment resulted in GlyT2 drug significant exacerbation of your eosinophil inflammation inside the airways of wild-type mice [88]. Therefore, CB2 receptor signaling in NK cells appears to become critical in treating allergic illnesses in the respiratory tract. Administering CBD in experimentally induced allergic asthma in mice limited the inflammatory procedure and airway remodeling primarily based on decreased collagen fibers and inflammatory markers [90]. Nevertheless, the results in the preclinical research are inconsistent and insufficient to draw unambiguous conclusions. Anti-inflammatory properties of CBD have also been documented in inflammation artificially induced by lipopolysaccharide in mice. Lung function improvement plus a reduce in leucocyte migration and decrease levels of inflammatory markers–such as TNF, IL-6, MCP-1, or MIP-2–have been reported [91]. Furthermore, it has been proved that CBD can reduce cytokine storms and includes a protective effect on lung tissue of mice with artificially induced acute respiratory distress syndrome (ARDS) [92]. There is a connection involving CBD administration as well as the regulation of apelin–a peptide displaying the protective impact on lung tissue [93]. Administration of THC also drastically attenuated the induced inflammation and also the immunological response within the airways in mice [94]. The effects had been observed even with simultaneous blockade or deficiency of CB1 and CB2 receptors, which points to equally relevant involvement of alternative paths of cannabinoids in mitigation on the inflammatory response [94]. In another study, authors proved the influence of THC in reducing the proliferation of immune cells and inhibiting the production of pro-inflammatory cytokines–such as IFN-, IL-1, IL-2, or TNF—in mice with airway inflammation induced by Staphylococcal enterotoxin B (SEB) [95]. Inside a similar study, treating experimental groups with THC led to decreased alveolar macrophages, neutrophils, lymphocytes CD4+, CD8+, NK, and NKT cells, regardless of the administered toxin [96]. Moreover, THC induces apoptosis of mononuclear cells infiltrating lungs and modifies the metabolism of T lymphocytes, which has been established based on reduction of cellular respiration in groups treated with THC, when compared with the manage group [96]. In addition, THC reduces the mortality of mice with ARDS induced by SEB [97]. Study shows the prospective of THC, as an anti-inflammatory agent, in treating cytokine storm and ARDS in sufferers suffering from COVID-19 [98]. However, adverse effects of cannabinoids on respiratory tract function in several pathological situations have also been documented [99,100]. Excessive stimulation of CB1 receptors could be associated with lung injury, inflammation, and fibrosis, also as improved pro-inflammatory cytokines and cyclooxygenase in the lungs [99].Molecules 2021, 26,12 ofCannabinoids unquestionably influence immunomodulatory processes in the respiratory tract, displaying substantial anti-inflammatory properties. However, activation of CB1 and CB2 receptors often presents contrary effects in pathological circumstances, which does not allow to figure out their exact distinct part inside the airways [99]. six. Cannabinoids inside the Neurological Problems The Chk1 Formulation expression of CB1 receptors is remarkably higher inside the central nervous method (CNS), specifically within the olfactory bulb, hippocampus, basal ganglia, and cerebellum [10.