IL-17RE/IL-17C mediate the recruitment of neutrophils during acute Streptococcus pneumoniae pneumonia

Neutrophils contribute to lung injury in acute pneumococcal pneumonia. The interleukin 17 receptor E (IL-17RE) is the functional receptor for the epithelial-derived cytokine IL-17C which is known to mediate innate immune functions. The aim of this study was to investigate the contribution of IL-17RE/IL-17C to pulmonary inflammation in a mouse model of acute Streptococcus pneumoniae pneumonia. Numbers of neutrophils, the expression of the cytokine granulocyte-colony stimulating factor (G-CSF), and tumor necrosis factor α (TNF-α) were decreased in lungs of IL-17RE deficient (Il-17re-/-) mice infected with S. pneumoniae. Numbers of alveolar macrophages rapidly declined in both wild-type (WT) and Il-17re-/- mice and recovered 72 hours after infection. There were no clear differences in the elimination of bacteria and numbers of blood granulocytes between infected WT and Il-17re-/- mice. The fractions of granulocyte-monocyte progenitors (GMPs) were significantly reduced in infected Il-17re-/- mice. Numbers of neutrophils were significantly reduced in lungs of mice deficient for IL-17C 24 hours after infection with S. pneumoniae. These data indicate that the IL-17C/IL-17RE-axis promotes the recruitment of neutrophils without affecting the recovery of alveolar macrophages in the acute phase of S. pneumoniae lung infection.