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 differentiate from myeloid precursor cells. IL-5 controls the development of eosinophils in the bone marrow.
  • Prior to their exit from the bone marrow, eosinophils produce many secondary granule proteins.
  • Eosinophils migrate to inflammatory sites in tissues in response to chemokines like CCL11, CCL24, CCL5,, and certain leukotrienes like leukotriene B4.
  • When eosinophils are activated, they release eosinophilic granules.
  • Following activation, eosinophils effector functions include production of reactive oxygen products such as superoxide and peroxide produced by eosinophil peroxidase, growth factors such as TGF beta and cytokines such as IL-1, IL-2, and TNF alpha.
  • These products cause direct cytotoxicity, upregulation of chemoattraction, expression of adhesion molecules, regulation of vascular permeability, and contraction of smooth muscle cells.7–9
  • 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

References

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