Abstract
Neuroimmune mechanisms and their role in the pathogenesis of asthma have been actively discussed in the scientific literature in recent years. There is emerging evidence of a relationship between neurotrophic factors and lipid metabolism in asthma. Despite the significance of existing research, the literature is insufficient to support a neuro-immune-lipid model of asthma that defines the pathogenetic relationship between these three systems. Brain-derived neurotrophic factor (BDNF) is implicated in the pathogenesis of bronchial hyperreactivity and remodeling, integrating the neuroimmune mechanisms of asthma pathogenesis. Lipid metabolism disturbances in asthma, including an imbalance of proinflammatory and anti-inflammatory lipid mediators, as well as changes in sphingolipid and cholesterol levels in cell membranes, can influence the expression of BDNF and its receptor, which form the BDNF/TrkB signaling pathway. This allows us to consider the relationship between lipids and neurotrophins as a mechanism linking metabolic dysregulation with neuroimmune inflammation and airway remodeling in asthma. In this mechanism, lipids are considered to act as mediators modulating BDNF activity by activating signaling pathways that regulate BDNF gene transcription. Further research will help substantiate a unified neuro-immune-lipid model of asthma pathogenesis.