Eosinophilic pneumonia pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Priyamvada Singh, M.D. [2]
Overview
Pathophysiology
Development of esopinophils
- Eosinophils are recruited in the blood and tissue, including the lung in response to circulating IL-5, eotaxins, and the C-C chemokine receptor-3 (CCR3).
- The prominence of IL-5 in eosinophil differentiation and recruitment has led to the development of anti–IL-5 monoclonal antibodies to selectively target the eosinophil lineage in humans with asthma.10–14
Eosinophils and Immunity
- Eosinophils interact with basophils, endothelial cells, macrophages, platelets, fibroblasts, and mast cells through cell membrane signaling molecules and receptors including Toll-like receptors and receptors for cytokines, immunoglobulins, and complement.7–9,15
- Activated eosinophils release proinflammatory cytokines, arachidonic acid– derived mediators, enzymes, reactive oxygen species, complement proteins, chemokines, chemoattractants, metalloproteases, and cationic proteins.
- The latter are released by degranulation of activated eosinophils and exert a variety of effects, including direct cytotoxicity, upregulation of chemoattraction, expression of adhesion molecules, regulation of vascular permeability, and contraction of smooth muscle cells.7–9
- Activated, degranulated eosinophils can be found in the bronchoalveolar lavage (BAL)16,17 and the lung tissue18 of patients with eosinophilic pneumonias.
- Tissue damage mediated by eosinophil cationic proteins is exemplified by the cardiac lesions that occur in the hypereosinophilic syndrome or in tropical eosinophilia.15 Eosinophils are also involved in adaptive immunity against bacteria, viruses, and tumors through interaction with T-lymphocytes.7–9 They present antigens to T-helper-2 cells in tissues and in the draining lymph nodes in the context of major histocompatibility complex class II, thereby inducing T cell development, activation, and migration to sites of inflammation.
- Eosinophils secrete IL-4 and IL-13, amplifying the T-helper-2 response in the lung, and in turn are recruited and activated by T-helper-2 cell-derived cytokines (IL-4, IL-5, and IL-13).