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* From "Marianthi Simou" Laboratory (Drs. Kalomenidis and Papiris), Department of Critical Care and Pulmonary Services, Athens Medical School, "Evangelismos" Hospital, Athens, Greece; Department of Respiratory and Critical Care Medicine (Dr. Guo), First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China; Pulmonary Medicine Department (Dr. Light), Saint Thomas Hospital, Department of Allergy, Pulmonary and Critical Care Medicine (Drs. Lane and Perebles), Vanderbilt University, Nashville, TN; and Section of Pulmonary and Critical Care Medicine (Dr. Elias), Department of Internal Medicine, Yale School of Medicine, New Haven, CT.
Correspondence to: Ioannis Kalomenidis, MD, Department of Critical Care and Pulmonary Services, Athens Medical School, "Evangelismos" Hospital, 4547 Ipsilandou Str., 10675 Athens, Greece; e-mail: jkalomenidis{at}hotmail.com
Study objectives: To establish a murine model of pneumothorax-associated pleural eosinophilia and to examine the role of interleukin (IL)-5 and IL-13 in the pathogenesis of this reaction.
Design: An animal study.
Interventions: One hundred thirty-seven C57/Bl-6 mice were used in this study. Wild-type animals were injected intrapleurally with 0.4 mL of air and were killed at different time points (30 min to 7 days) after the injection. IL-5 knockout and IL-13 knockout animals were killed 24 h and 48 h after the injection. Pleural inflammation was assessed by pleural lavage (PL).
Measurements and results: PL cells were significantly increased following the induction of pneumothorax. The peak number of neutrophils, observed at 12 h, was 900 times higher than the control. The peak number of eosinophils, observed at 48 h, was 700 times higher than the control. Lymphocytes and mononuclear cells increased threefold and fourfold, respectively. IL-5 knockout mice had significantly less PL eosinophils than that the wild-type or the IL-13 knockout mice at 24 h (150 ± 46/µL, 903 ± 244/µL, and 912 ± 168/µL, respectively; p = 0.013) and 48 h (181 ± 45/µL, 1,587 ± 212/µL, and 1,379 ± 364/µL, respectively; p = 0.003).
Conclusion: Pneumothorax induces an inflammatory reaction of the mouse pleura, mainly characterized by increased neutrophils and eosinophils. IL-5 but not IL-13 is required for pneumothorax-associated pleural eosinophilia.
Key Words: animal model eosinophils interleukin-5 interleukin-13 pleura pneumothorax
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