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IL-5 in post-traumatic eosinophilic pleural effusion

L Schandené¹, B Namias, A Crusiaux

¹Department of Immunology-Haematology, Hôpital Erasme, Université Libre de Bruxelles, Belgium.

Clinical and Experimental Immunology

|July 1, 1993

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Post-traumatic pleural fluid eosinophilia is linked to Interleukin-5 (IL-5). This cytokine is locally produced by CD4+ cells in the pleural cavity, driving eosinophilic pleural effusions (EPE).

Area of Science:

Immunology
Pulmonology
Cell Biology

Background:

Thoracic trauma and pneumothorax can lead to pleural fluid eosinophilia.
Eosinophilic pleural effusions (EPE) are a recognized, though less common, complication of thoracic injuries.

Purpose of the Study:

To investigate the role of the eosinophilopoietic cytokine Interleukin-5 (IL-5) in the development of post-traumatic EPE.
To determine the source and bioactivity of IL-5 in EPE.

Main Methods:

Immunoenzymatic assay to quantify IL-5 levels in pleural fluid and serum.
Bioactivity assay using a mouse CTLL-2 cell line.
Reverse polymerase chain reaction (PCR) to detect IL-5 mRNA expression in pleural mononuclear cells and peripheral blood mononuclear cells (PBMC).

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Purification and analysis of pleural CD4+ cells.

Main Results:

Significant levels of IL-5 were detected in EPE fluids, but not in serum or non-eosinophilic pleural fluids.
Pleural IL-5 was bioactive, stimulating cell proliferation.
IL-5 mRNA was expressed by pleural mononuclear cells, but not PBMC, indicating local synthesis.
Pleural CD4+ cells were identified as the primary source of IL-5.

Conclusions:

Local secretion of IL-5 by pleural CD4+ cells plays a crucial role in the pathogenesis of post-traumatic EPE.
IL-5 is a key mediator driving eosinophil accumulation in the pleural space following trauma.