“…Asthma is characterized by non-specific respiratory symptoms such as wheezing, shortness of breath, chest tightness, and episodic cough as the main clinical manifestations, which frequently occur at night and early in the morning, and its main pathogenesis is chronic immune-inflammatory response, airway hyperreactivity, reversible airflow limitation, and airway remodeling ( 6 , 7 ). Patients with asthma are often accompanied by neurological symptoms such as cognitive dysfunction, depression, anxiety, dysosmia, and sleep disorders, implying a brain response to asthma, which affects their quality of life, increases their economic burden, reduces the treatment sensitivity of asthma, increases the risk of asthma exacerbations, and forms a vicious cycle ( 8 – 10 ). Based on our previous summary of brain response in allergic rhinitis (AR) ( 11 ), a “lung–brain” crosstalk in asthma can be observed on the basis of neuro-immune mechanisms, that is, inflammatory factors generated during chronic inflammation in asthma can be transmitted upwards to the central nervous system, thereby stimulating associated brain regions to elicit one or more brain responses, transmitting response commands to peripheral nerves, activating such commands to release mediators such as neuropeptides and neurogenic trophic factors, worsening asthma symptoms through actions such as tracheal smooth muscle contraction, promoting the re-entry of immune inflammatory factors produced in the periphery to the brain, and exacerbating neurological symptoms caused by brain response ( 12 , 13 ).…”