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Characterisation of pleural inflammation occurring after primary spontaneous pneumothorax

Respiratory Division and Haematology-Immunology Dept, Academic Hospital, Brussels, Belgium

CORRESPONDENCE: M. Noppen, Respiratory Division, Academic Hospital, Academisch Ziekenhuis Vrije universiteit Brussel, 101 Laarbeeklaan, B-1090 Brussels, Belgium. Fax: 32 2477684, E-mail: marc.noppen@az.vub.ac.be

Keywords: Cytokines, eosinophils, inflammation, pleural lavage, pneumothorax, primary spontaneous.

Received: July 9, 2003
Accepted February 11, 2004

The Dept of Internal Medicine and the Respiratory Division of the Academic Hospital AZ-VUB supported this work

The aim of this study was to examine the inflammatory reaction occurring in the pleural space of patients suffering from primary spontaneous pneumothorax (PSP) using pleural lavage, which was performed in patients with PSP and in healthy control subjects (essential hyperhidrosis patients undergoing thoracoscopy for sympathicolysis treatment). Cellular and solute composition of lavage fluid, peripheral blood and parietal pleural biopsies were analysed.

PSP lavage fluid showed an increase in all differentiated leucocytes, but most strikingly eosinophils and neutrophils. In the blood of patients with PSP, the total number of leucocytes and the absolute number of eosinophils, neutrophils and monocytes were also significantly increased. The time in which air was present in the pleural space was positively correlated with the increase of eosinophils in lavage fluid, parietal pleura and blood. Eosinophilic cationic protein was elevated after PSP and strongly correlated with the absolute number of lavage eosinophils. Chemo and cytokine analysis in lavage fluid showed differences in concentrations of interleukin (IL)-5, IL-6, IL-8, IL-12p40, tumour necrosis factor- and RANTES, but not of eotaxin. Surprisingly, high levels of lipopolysaccharide binding protein were also measured.

Primary spontaneous pnumothorax is associated with a substantial pleural inflammatory reaction. The authors hypothesise that mechanical stretch factors, lipopolysaccharide binding protein/lipopolysaccharide complexes or other environmental components trigger pleural inflammation after primary spontaneous pnumothorax.

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