Eosinophilic pneumonia pathophysiology: Difference between revisions

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Revision as of 21:06, 11 February 2018

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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 == Pathophysiology ==
-==== Development of esopinophils ====
+=== 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).
+* Eosinophils differentiate from myeloid precursor cells. IL-5 controls the development of eosinophils in the bone marrow.
-* 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
+* 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.
-==== Eosinophils and Immunity ====
+* When eosinophils are activated, they release eosinophilic granules.
-* 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
+* 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.
-* Activated eosinophils release proinflammatory cytokines, arachidonic acid– derived mediators, enzymes, reactive oxygen species, complement proteins, chemokines, chemoattractants, metalloproteases, and cationic proteins.
+* These products cause direct cytotoxicity, upregulation of chemoattraction, expression of adhesion molecules, regulation of vascular permeability, and contraction of smooth muscle cells.7–9
-* 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
+* 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, 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).
 ==References==

Eosinophilic pneumonia pathophysiology: Difference between revisions

Revision as of 21:06, 11 February 2018

Overview

Pathophysiology

Development of esopinophils

References

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