Air in the pleural space is among the most common etiologies of eosinophilic pleural effusions (EPE). We have recently developed a mouse model of pneumothorax-induced pleural eosinophilia to examine the mechanisms of eosinophil accumulation in pleural tissues. In the present study we examined the significance of IL-5 and IL-13 in
Nine wild-type (wt), 6 IL-5 knockout and 4 IL-13 knockout C57/BL-6 mice where injected intrapleurally with 0.4 ml air. Mice were sacrificed 48 hours after the introduction of pneumothorax because, as we have previously shown, pleural eosinophilia peaks at this time point. Pleural lavage (PL) with 1 ml saline was performed immediately after death. Nucleated cell counts were measured with an automatic cell counter. Cytospins were made and stained with Wright-Giemsa stain for the differential cell count.
The mean ± SEM PL eosinophil counts were: 1799±188/mm3 in the wt group, 215±53/mm3 in the IL-5 knockout group and 1544±626/mm3 in the IL-13 knockout group. The mean ± SEM PL eosinophil percentages were 33±3.6%, 4.8±1.1% and 26±4.9%, respectively. The PL eosinophil counts and percentages were significantly lower in the IL-5 knockout mice than in the wt (p<0.001, for both the counts and the percentages), or the IL-13 knockout mice (p=0.001, for the percentage and p=0.03 for the counts). However, the PL eosinophil counts and percentages did not differ significantly between wt and IL-13 knockout mice.
IL-5 but not IL-13 is a crucial mediator of pneumothorax-associated pleural eosinophilia.
Anti-IL-5 treatment may be useful in the treatment of persistent, symptomatic post-traumatic eosinophilic pleural effusions.
I.T. Kalomenidis, None.