Published ahead of print on May 18, 2005, doi:10.1165/rcmb.2004-0213OC Am. J. Respir. Cell Mol. Biol., Volume 33, Number 3, September 2005, 248-253 A more recent version of this article appeared on September 1, 2005
Submitted on July 5, 2004 IL-17 as a Recruitment and Survival Factor for Airway Macrophages in Allergic Airway InflammationSvetlana Sergejeva1*,1 The Lung Pharmacology Group, Department of Respiratory Medicine and Allergology , Institute of Internal Medicine, Sahlgrenska Academy at Goteborg University, Gothenburg, Sweden; The Unit for Lung Investigations, National Institute for Health Development, Tallinn, Estonia, 2 The Lung Pharmacology Group, Department of Respiratory Medicine and Allergology , Institute of Internal Medicine, Sahlgrenska Academy at Goteborg University, Gothenburg, Sweden * To whom correspondence should be addressed. E-mail: Svetlana.Sergejeva{at}lungall.gu.se.
Recent data indicate that the pro-inflammatory cytokine, IL-17, stimulates certain effector functions of human macrophages. We evaluated whether IL-17 mediates allergen-induced accumulation of airway macrophages and, if so, whether such an effect relates to the control of macrophage recruitment and survival. BALB/c mice were sensitized and challenged with ovalbumin. Three hours before challenge an anti-mouse IL-17 mAb (a-IL-17) was administered. Sampling was conducted 24h after the allergen challenge. In vitro chemotaxis assay for blood monocytes and culture of airway macrophages, immunocytochemistry for Fas-antigen and matrix metalloproteinase-9 (MMP-9) were utilized to determine the IL-17's effects on the recruitment, survival and activity of airway macrophages. A-IL-17 reduced the number of airway neutrophils and macrophages after allergen challenge. In vitro, recombinant IL-17 induced migration of blood monocytes and prolonged survival of airway macrophages. A-IL-17 also increased the expression of Fas-antigen in airway macrophages in vivo. Finally, the expression of MMP-9 by airway neutrophils and macrophages in vivo was down-regulated by a-IL-17. This study indicates that endogenous IL-17 mediates the accumulation of macrophages during allergen-induced airway inflammation. IL-17 exerts its effects by acting directly on airway macrophages by promoting their recruitment and survival. Furthermore, IL-17 is involved in controlling the proteolytic activity of macrophages and neutrophils in allergen-induced airway inflammation.
This article has been cited by other articles:
|
|||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
