Allergic asthma is a heterogeneous respiratory disease characterized by chronic airway inflammation and immune disorder by an intricate interplay of genetic and environmental factors. The imbalance of pulmonary macrophage polarization acts as a pivotal driver of airway inflammatory remodeling and pathological injury. Pulmonary macrophages including alveolar macrophages (AMs) and interstitial macrophages (IMs) undergo remarkable metabolic reprogramming in the microenvironment of allergic asthma. The dynamic remodeling of core metabolic pathways including glycolysis, fatty acid, and amino acid metabolism is closely associated with M1/M2 phenotypic transition and functional plasticity of macrophages. Meanwhile, metabolic enzymes, key metabolic intermediates and transcriptional regulators bidirectionally modulate macrophage polarization via epigenetic modification and signaling pathway activation. In turn, the activation and polarization of macrophages further reshape cellular metabolic patterns, forming a closed loop of metabolism-immunity interaction. This review systematically summarizes the characteristics and regulatory mechanisms of pulmonary macrophage polarization in allergic asthma, focuses on elucidating the crosstalk regulatory network between metabolic reprogramming and macrophage functional plasticity, and clarifies the roles of key metabolic pathways in airway inflammation, airway hyperresponsiveness and tissue remodeling in asthma. We also summarize that the pharmacological manipulation of macrophage glucose and lipid metabolism can effectively attenuate airway hyperresponsiveness and structural remodeling, highlighting that immunometabolic pathway serve as promising therapeutic targets for asthma intervention.
Huang et al. (Fri,) studied this question.
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