Pathogenesis of the eosinophilic pleural effusions.
OBJECTIVE
Eosinophilic pleural effusions (EPE) are defined as those that contain at least 10% eosinophils. EPEs account for 5 to 16% of exudative pleural effusions. However, their pathogenesis is poorly understood. The purpose of this review is to discuss the mechanisms that lead to eosinophilic pleural inflammation.


RESULTS
Eosinophilic pleural effusions are caused by the presence of air or blood or both in the pleural space, infectious or other inflammatory diseases, malignancy, pulmonary emboli, asbestos exposure, and drug reactions. Differences in the clinical features suggest that a variety of mechanisms operate to induce eosinophilic pleural inflammation and pleural fluid accumulation. Human and animal studies indicate that interleukin (IL)-5 is an important common contributor of different pathogenetic pathways. The possible role of other cytokines, chemokines, and adhesion molecules in the development of EPE is under investigation.


CONCLUSIONS
Understanding the pathogenesis of EPE will permit the development of novel therapies for the persistent, symptomatic, posttraumatic and idiopathic EPE. Anti-IL-5 treatment is an interesting option that requires further research.
Kalomenidis
Ioannis
I
Department of Critical Care and Pulmonary Services, Evangelismos Hospital, Athens Medical School, Athens, Greece. jkalomenidis@hotmail.com
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Richard W
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D000818:Animals; D002448:Cell Adhesion / Q000502:physiology; D018925:Chemokines / Q000276:immunology; D016207:Cytokines / Q000276:immunology; D004195:Disease Models, Animal; D004802:Eosinophilia / Q000209:etiology* / Q000276:immunology / Q000473:pathology; D004804:Eosinophils / Q000276:immunology / Q000473:pathology*; D006801:Humans; D015848:Interleukin-5 / Q000276:immunology; D010996:Pleural Effusion / Q000209:etiology* / Q000276:immunology / Q000473:pathology
D018925:Chemokines; D016207:Cytokines; D015848:Interleukin-5