Eosinophils are differentiated from bone marrow hematopoietic stem cells, and the differentiation process is regulated by interleukin-3 (IL-3), interleukin-5 (IL-5), and granulocyte macrophage colony-stimulating factor (GM-CSF), with IL-5 also regulating the release and migration of eosinophils from the bone marrow to tissues after maturation. Once activated, eosinophils can rapidly release large amounts of pre-synthesized inflammatory mediators, including major basic protein (MBP), eosinophil-derived neurotoxin (EDN), and eosinophilic cationic protein (ECP), which can trigger an inflammatory response in tissues. Peripheral blood eosinophilia is classified according to different degrees: mild (500C1500/mm3), moderate (1500C5000/mm3), and severe (>5000/mm3). It is important to note that increased eosinophilia in the peripheral blood does not necessarily represent the degree of cellular infiltration in the tissues, and in addition, increased numbers do not necessarily mean increased cellular activity. Common causes of eosinophilia include: 1. Drug factors. In low endemic areas of parasitic infection, drug factors are the most common cause of eosinophilia. After drug-associated eosinophilia occurs, the need for medication, the feasibility of alternative medications, and end-organ involvement need to be evaluated; it is not necessary to discontinue medication when the disease is mild. Once end-organ involvement is evident, such as eosinophilic pulmonary infiltrates caused by salazosulfapyridine, penicillins/cephalosporins, and non-steroidal anti-inflammatory drugs (NSAIDs), and acute interstitial nephritis, immediate discontinuation of the drug and supportive treatment of the affected organ is required. Drug-induced hypersensitivity syndrome (DIHS) usually develops 4-12 weeks after initiation of the drug and symptoms can persist for several weeks even after discontinuation of the drug. It is important to note that the cause of DIHS is not limited to drugs, but can also be triggered by reactivation of latent viruses (e.g., human herpes virus types 6 and 7, EBV, and cytomegalovirus). 2. Allergic diseases. Eosinophilia due to common allergic diseases is usually not higher than 1500/mm3, but severe atopic dermatitis, severe asthma, nasal polyposis, and allergic bronchopulmonary aspergillosis (ABPA)/allergic bronchopulmonary fungal disease (ABPM) can cause a significant increase in eosinophils. Eosinophilic granulomatous vasculitis, manifesting as necrotizing vasculitis and extravascular granulomatous, can be associated with asthma and significantly increased eosinophils. 40% of these patients are associated with positive ANCA, manifesting as necrotizing glomerulonephritis, pulmonary hemorrhage, and polyneuritis moniliformis; other ANCA-negative patients show more pronounced tissue infiltrates, such as eosinophilic gastritis/enteritis. 3. Infectious factors, including parasites, viruses, and fungi. Tissue-invasive parasitic infections are the most common cause of eosinophilia worldwide. Bacterial infections usually result in lower peripheral blood eosinophils, so finding a bacterial infection with eosinophilia needs to be evaluated for other causes, such as whether it is caused by antibiotics used to treat the infection. Bronchial epithelial cell viral infections can lead to the release of multiple inflammatory mediators and the recruitment of immune cells (eosinophils, neutrophils, and mast cells) to further release more inflammatory mediators and produce airway inflammation. Respiratory viral infections in children can lead to recurrent wheezing, and some studies have shown that eosinophils can promote clearance of respiratory viruses. Therefore, if eosinophils are found to be elevated in children with respiratory infections, this often suggests that the body is clearing the virus and not necessarily an allergic reaction. 4. Tumors. Tumor necrosis can lead to increased eosinophil chemotactic response, and tumor cell spread can also lead to increased eosinophil production in the bone marrow, and if the tumor itself can produce large amounts of eosinophil proteins, such as IL-3, IL-5, and GM-CSF, it can cause increased eosinophils. In addition, myeloid and lymphatic blood malignancies are also the cause of increased eosinophil production. 5. Endocrine factors. Diseases such as Addison’s disease, adrenal hemorrhage and hypopituitarism can lead to a decrease in the production of endogenous adrenal glucocorticoids, resulting in an increase in peripheral blood eosinophils. 6. Other diseases. Examples include rheumatic diseases, systemic mastocytosis (>650 /mm3 in up to 28% of patients), congenital immunodeficiency (e.g. severe atopic dermatitis with significantly elevated eosinophils, often suggesting hyper IgE syndrome or Omenn syndrome) 7. Hypereosinophilia. The diagnostic criteria used since 1975 include: (1) peripheral blood eosinophils ≥1500/mm3 for more than 6 months, or death within 6 months; (2) except for other possible causes of eosinophilia, such as parasitic infections, allergic diseases, etc.; (3) signs of organ involvement, such as heart failure, gastrointestinal dysfunction, central nervous system (3) signs of organ involvement such as heart failure, gastrointestinal dysfunction, central nervous system abnormalities, fever, weight loss, etc. With the advancement of medical understanding, the 2006 diagnostic criteria added exclusionary etiologies: eosinophilic gastrointestinal disease (EGID), eosinophilic granulomatous vasculitis (EGPA), and chronic eosinophilic pneumonia. Further, considering that peripheral blood eosinophils are not fully representative of the degree of infiltration in the tissues, the currently used diagnostic criterion deleted “persisting for more than 6 months” and replaced it with “at least two episodes of peripheral blood eosinophils ≥1500/mm3 within 6 months “. The common treatment for eosinophilia is glucocorticoids, and care should be taken to avoid side effects such as diabetes, hypertension, osteoporosis, cataracts, glaucoma, myopathy, and depression. The American College of Rheumatologists (ACR) recommends long-term treatment with glucocorticoids along with: (1) supplemental calcium intake of 1200 mg/day and vitamin D intake of 800 IU/day; (2) regular bone density scans; and (3) diphosphonate therapy for all patients at high risk for long-term use (≥3 months), postmenopausal women, and men ≥50 years of age. In recent years, molecular therapies have become increasingly available, and monotherapy with anti-interleukin 5 and anti-interleukin 5 receptor alpha chains is gradually being extended to other eosinophilic diseases other than bronchial asthma, such as hypereosinophilia and eosinophilic granulomatous vasculitis, with remarkable efficacy.