Neutrophil Recruitment by Interleukin-17 into Rat Airways In Vivo

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Abstract
We determined whether neutrophil recruitment induced by the T-lymphocyte cytokine, interleukin-17 (IL-17) is modulated by tachykinins in airways in vivo. Cell recruitment into airways was induced by either human (h) IL-17 (1 μ g) or rat (r) IL-1 β (2.5 ng), instilled intratracheally in rats (n = 5 to 7). Six hours after instillation, hIL-17 (3.1 ± 1.2 × 106 cells/ml) and rIL-1 β (4.1 ± 0.5 × 106 cells/ml), respectively, induced a significant and selective increase in neutrophil count in bronchoalveolar lavage fluid (BAL) when compared with vehicle (0.6 ± 0.2 × 106 cells/ml). For hIL-17, this effect was dose-dependent. Inhalation of peptidase inhibitors (phosphoramidon plus captopril) potentiated the effect of both hIL-17 and rIL-1 β . Inhalation of a neutral endopeptidase inhibitor (phosphoramidon) alone also increased the neutrophil count for hIL-17, whereas an angiotensin-converting enzyme inhibitor (captopril) alone did not. A selective neurokinin (NK)-1 receptor antagonist (SR 140333) reduced the neutrophil count, both with and without phosphoramidon pretreatment. In conclusion, IL-17 selectively recruits neutrophils into rat airways in vivo and this effect is modulated by endogenous tachykinins acting via NK-1 receptors.