Eosinophilic Interstitial Pneumonia

The study of the biologic role played by eosinophils in health and disease starts with the first description of these cells made by Ehrlich in 1879. Eosinophils develop in the bone marrow from CD34+ progenitor cells. The presence of a specific cytokine milieu drives their terminal differentiation into mature eosinophils. Normally, there are virtually no eosinophils in the lungs. Different stimuli, originating from inflamed tissues, may attract eosinophils from the blood into the airway and lung parenchyma. Eosinophils activated by local signals, exert their biological action through the release of the content of their granules and is harmful for lung tissue. Their granule products activate lung macrophages, stimulate mast cells, induce airway smooth muscle contraction and may also damage airway epithelium, altering its permeability and increasing mucus production. This article describes acute and chronic eosinophilic pneumonia, eosinophilic granulomatosis with polyangiitis, hypereosinophilic syndromes and drug related hypereosinophilia. These diseases have in common an immune-inflammatory process leading to the recruitment and activation of eosinophils. The subsequent release of eosinophil-derived proteins, causing lung damage, determines disease conditions all characterized by the pathogenic role of eosinophils.