Paul Ehrlich discovered and called human eosinophils in 1879 based on the cell’s granular eosin uptake. Although eosinophils account for just around 1% of peripheral blood leukocytes, they have a proclivity to exit the bloodstream and move into inflammatory tissues. Asthma and eosinophilic granulomatosis with polyangiitis rely heavily on eosinophils and their mediators (EGPA). Eosinophils have a plethora of cell-surface receptors and generate a variety of cytokines and chemokines. Eosinophils are the primary source of interleukin-5 and have a high level of interleukin-5R expression on their surface. In patients with eosinophilic asthma, EGPA, and chronic obstructive pulmonary disease, clinical studies testing monoclonal antibodies against interleukin-5 and its receptor interleukin-5R have been conducted or are now underway (COPD). Targeting interleukin-5/interleukin-5R is linked with a significant reduction in blood and sputum eosinophilia, a reduction in the number of exacerbations, and improvement in several clinical indicators in adult patients with severe eosinophilic asthma. Pilot trials indicate that mepolizumab may be a glucocorticoid-sparing therapy in EGPA patients. Benralizumab did not reduce exacerbations but did improve lung function in individuals with eosinophilic COPD, according to early research.
The study looks at recent discoveries in eosinophil biology and how targeting the interleukin-5 pathway might help certain individuals with severe asthma, EGPA, and COPD. Interleukin-5/interleukin-5R-targeted therapies provide hope for individuals suffering from eosinophilic respiratory diseases.
