Interleukin (IL)-17 can recruit neutrophils (PMNs) through indirect mechanisms and thereby contribute to pulmonary host defense. IL-17 may induce PMN apoptosis as well; and this through a direct mechanism (Silverpil et al, EAACI 2007). We now determined whether IL-17-induced PMN apoptosis is associated with increased bactericidal activity.


Blood PMNs from Balb/c mice were isolated and cultured in vitro (48 hrs) in medium with mouse recombinant IL-17 protein (1-100 ng/mL) or in medium alone (control). Apoptosis and necrosis of the PMNs were measured on a flow cytometer targeting Annexin V and 7AAD, whereas the bactericidal activity was assessed by measuring extracellular myeloperoxidase (MPO) in the conditioned medium using ELISA. Data shown as (mean [SEM]), n=4-6.


IL-17 increased PMN apoptosis (Annexin V+, 7AAD-) from 34 [1] % in the control group to a maximum of 55 [8] % (p< 0.05, Mann-Whitney U-test), but it did not affect PMN necrosis (Annexin V+, 7AAD+, not shown). The MPO concentration correlated positively with PMN apoptosis (p<0.01, Spearman's rank correlation).


This study demonstrates that IL-17-induced PMN apoptosis correlates with MPO release in vitro. This finding suggests that IL-17 is involved in terminating the innate component of pulmonary host defense in a controlled manner, while at the same time maintaining bactericidal activity.