title: Pneumothorax-associated pleural eosinophilia is tumour necrosis factor-alpha-dependent and attenuated by steroids.
abstract: OBJECTIVE
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Applied Biomedical Research and Training Center Marianthi Simou, Department of Critical Care and Pulmonary Services, Athens Medical School, Evangelismos Hospital, Athens, Greece. ikalom@med.uoa.gr
authors.forename: Ioannis
authors.initials: I
authors.lastname: Kalomenidis
authors.forename: Charalampos
authors.initials: C
authors.lastname: Moschos
authors.forename: Androniki
authors.initials: A
authors.lastname: Kollintza
authors.forename: Ioanna
authors.initials: I
authors.lastname: Sigala
authors.forename: Georgios T
authors.initials: GT
authors.lastname: Stathopoulos
authors.forename: Spyros A
authors.initials: SA
authors.lastname: Papiris
authors.forename: Richard W
authors.initials: RW
authors.lastname: Light
authors.forename: Charis
authors.initials: C
authors.lastname: Roussos
mesh_terms: D000818:Animals; D003907:Dexamethasone / Q000627:therapeutic use*; D004195:Disease Models, Animal; D004802:Eosinophilia / Q000188:drug therapy* / Q000209:etiology / Q000378:metabolism*; D005938:Glucocorticoids / Q000627:therapeutic use*; D015848:Interleukin-5 / Q000378:metabolism; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D011030:Pneumothorax / Q000150:complications* / Q000378:metabolism / Q000473:pathology; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology*
chemical_list: D005938:Glucocorticoids; D015848:Interleukin-5; D014409:Tumor Necrosis Factor-alpha; D003907:Dexamethasone