Bronchial asthma is a chronic inflammatory disease of the airways in which multiple inflammatory cells and cytokines are involved, and one of its key features is the large number of eosinophils that can be present in the airway lumen. Eosinophil infiltration and activation can occur even locally in the airways of mild to moderate asthma and is closely associated with bronchial epithelial damage and airway hyperresponsiveness. There is increasing evidence that cytokines produced by T lymphocytes are involved in regulating the recruitment and activation of eosinophils and other biological effects, the most interesting of which is the production of interleukin (IL)-5 by Th2 cells. IL-5 also selectively enhances eosinophil degranulation and antibody-dependent cytotoxicity, and enhances their adhesion to the vascular endothelium. Subsequent animal studies confirmed that anti-IL-5 monoclonal antibodies suppressed pulmonary eosinophil infiltration and airway hyperresponsiveness over time, and IL-5 knockout mice did not develop eosinophilia and airway hyperresponsiveness after allergen excitation. In humans, large numbers of eosinophils are mobilized to infiltrate the airways and are activated after IL-5 inhalation in asthmatics. In addition, IL-5 can contribute to increased airway responsiveness in patients with allergic asthma by a mechanism related to the activation of eosinophils to release toxic proteins. Mepolizumab is a synthetic high-affinity, complement-free binding human IL-5-specific antibody (IgG1) that blocks the action of IL-5 by binding to the A chain of the IL-5 receptor complex on the surface of eosinophils.Leckie et al. looked at the therapeutic efficacy of anti-IL-5 monoclonal antibodies in allergen-induced airway hyperresponsiveness and airway inflammation. Flood-Page et al. showed that although application of IL-5 antibody significantly reduced eosinophils in blood and airways, it had no effect on allergen response and airway hyperresponsiveness. after 20 weeks of treatment with triple doses of mepolizumab in patients with mild asthma, it still only partially reduced eosinophils in the airway tissue of asthmatic patients but did not achieve complete eradication. A multicenter, randomized, double-blind, placebo-controlled clinical trial evaluating the efficacy of intravenous mepolizumab in refractory asthma showed that 250 and 750 mg of mepolizumab significantly reduced eosinophils in circulating blood and sputum compared with placebo, but did not improve FEV1 or asthma symptom scores. This result suggests that in patients with refractory asthma, anti-IL-5 treatment does not improve their lung function and asthma symptoms; and, consistent with the findings of Leckie et al [14], mepolizumab had no effect on allergen response and airway hyperresponsiveness; in another trial, the investigators switched to other anti-human IL-5 antibodies and the results remained the same. Given this, the investigators hypothesized that eosinophils are not the key cells in the delayed asthma response and that their presence or absence does not affect the course of asthma. In patients who did not inhale cortisol hormone, the study showed that mepolizumab treatment was ineffective, but it must be noted that flaws in the trial’s parallel control group design and the lack of a validated study endpoint influenced the judgment of the trial’s results. Previous trials of mepolizumab for mild to moderate asthma have been short and negative, making it impossible to assess the efficacy of the drug for frequent asthma exacerbations. Haldar et al. conducted a randomized, double-blind, parallel, placebo-controlled clinical study and showed that mepolizumab significantly reduced the number of acute asthma exacerbations over 50 weeks, significantly improved the Asthma Quality of Life Questionnaire scores, and significantly reduced eosinophils in peripheral blood and sputum compared to the placebo group. Nair et al. also conducted a randomized double-blind parallel trial with a control group of patients with asthma symptoms and persistent eosinophils in sputum despite the use of prednisone, and showed that mepolizumab not only reduced the number of eosinophils in the peripheral blood and sputum of patients, but also reduced the dosage of cortisol hormone in such patients. Unlike previous studies on anti-IL-5 antibodies, the number of eosinophils was somewhat higher in the subjects in the new study. However, there was no significant improvement in asthma symptoms or FEV1 after mepolizumab application, except for a reduction in eosinophil counts. In contrast, corticosteroids produced a broader anti-inflammatory effect to control asthma and were not dependent on the effect of mepolizumab. This phenomenon implies that eosinophils are not the only ones involved in the pathogenesis of asthma. The above-mentioned studies show that eosinophils play an important role in the pathogenesis of some patients with bronchial asthma and that treatment with anti-IL-5 antibodies can achieve some clinical efficacy.