Pneumothorax-associated pleural eosinophilia is tumour necrosis factor-alpha-dependent and attenuated by steroids.

Background And Objectives: The pathogenesis and the optimal treatment of eosinophilic pleural effusions are unknown. We aimed to examine whether pneumothorax-associated pleural eosinophilia in mice is dependent on tumour necrosis factor (TNF)-alpha, and whether it is affected by systemic administration of corticosteroids.

Methods: Mice were injected intrapleurally with 0.4 mL air to create pneumothoraces. Animals were sacrificed 24 or 48 h later, and pleural lavage (PL) was performed. In the first experiment, comparisons were made between wild-type and TNF-alpha knockout mice with pneumothorax. In the second experiment, wild-type mice were injected intraperitoneally with different doses of dexamethasone (0, 0.25, 0.5 and 1 mg/kg), 5 min before and 24 h after the induction of pneumothorax.

Results: After induction of a pneumothorax, TNF-alpha knockout mice had significantly fewer total number of cells (P = 0.004), mononuclear cells (P = 0.01), neutrophils (P = 0.017) and eosinophils (P = 0.002) in their PL compared with wild-type animals. TNF-alpha was detected in the PL of most of the control mice but not in TNF-alpha knockouts. Dexamethasone induced a significant, dose-dependent reduction of PL total cells (P < 0.001), eosinophils (P < 0.001), mononuclear cells (P = 0.007) and lymphocytes (P = 0.04) at 48 h, and significantly reduced the number of PL total cells (P = 0.045) and eosinophils (P = 0.005) at 24 h. Furthermore, dexamethasone prevented eosinophil infiltration of lung and pleural tissue.

Conclusion: Pneumothorax-associated pleural eosinophilia in mice is TNF-alpha-dependent and is significantly attenuated by corticosteroid treatment. In addition, both TNF-alpha deficiency and dexamethasone treatment were associated with a significant reduction of other types of inflammatory cells in PL.