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1 Lung Pharmacology Group, Dept of Respiratory Medicine and Allergology, Institute of Internal Medicine and 2 Dept of Clinical Immunology, Göteborg University, Gothenburg, Sweden. 3 First Dept of Internal Medicine, Yokohama City University School of Medicine, Yokohama, Japan
CORRESPONDENCE: A. Lindén, Lung Pharmacology Group, Guldhedsgatan 10A, S-413 46, Gothenburg, Sweden. Fax: 46 31413290. E-mail: anders.linden@lungall.gu.se
Keywords: airway, cytokine, lymphocyte, neutrophil, recruitment, survival
Received: December 15, 2001
Accepted September 19, 2002
This study was supported by Herman Krefting's Foundation, the Swedish Medical Research Council (K2002-74X-09048-13A), the Vardal Foundation and the Swedish Heart Lung Foundation. No support, direct or indirect, was obtained from the tobacco industry.
Abstract
The T-cell cytokine interleukin (IL)-17 selectively accumulates neutrophils in murine airways in vivo and may thus constitute a link between activation of T-lymphocytes and accumulation of neutrophils. In this study, the authors evaluated the role of granulocyte macrophage-colony stimulating factor (GM-CSF) in accumulation of neutrophils in the airways caused by IL-17 and tumour necrosis factor (TNF)-
In vitro, human (h) IL-17 concentration-dependently stimulated the release of GM-CSF protein (enzyme-linked immunosorbent assay) in human bronchial epithelial cells (16HBE). IL-17 also time-dependently stimulated the release of GM-CSF protein in venous endothelial (human umbilical vein endothelial cells) cells in vitro. Co-stimulation with IL-17 plus the pro-inflammatory cytokine TNF-
In conclusion, granulocyte macrophage-colony stimulating factor is involved in the accumulation of neutrophils in the airways caused by interleukin-17 and tumour necrosis factor-
. potentiated the release of GM-CSF protein in 16HBE cells. hIL-17 also enhanced the expression of GM-CSF messenger ribonucleic acid in 16HBE cells (reverse transcriptase polymerase chain reaction), with a similar order of magnitude as TNF-. Conditioned cell medium from bronchial epithelial cells co-stimulated with hIL-17 plus TNF- prolonged survival (trypan blue exclusion) of human neutrophils in vitro and this effect was blocked by an anti-GM-CSF antibody. In vivo, local co-stimulation with mouse IL-17 plus TNF- caused an additive potentiation of the accumulation of neutrophils in bronchoalveolar lavage fluid from mouse airways and this effect was blocked by an anti-GM-CSF antibody given systemically. , probably via effects on both recruitment and survival of neutrophils.
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