In asthma models and patient-derived monocyte-derived macrophages facing concurrent respiratory infection, exposure to fatty acids intensifies LDHA expression and lactate production, heightening glycolysis and driving excessive TNF-α, IL-6, IL-1β and NO release; the glycolytic antagonist 2-deoxyglucose (2-DG) reverses these pro-inflammatory effects (Xuan et al., 2024). The gene discussed is IL1B; the disease is respiratory tract infectious disorder.