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Localization and Enhanced mRNA Expression of the Orphan Chemokine Receptor L-CCR in the Lung in a Murine Model of Ovalbumin-induced Airway Inflammation

Jaap Oostendorp, Machteld N. Hylkema, Marjan Luinge, Marie Geerlings, Herman Meurs, Wim Timens, Johan Zaagsma, Dirkje S. Postma, Hendrikus W. Boddeke and Knut Biber

Departments of Molecular Pharmacology (JO,HM,JZ), Pulmonology (JO,ML,MG,DSP), Pathology (MNH,ML,MG,WT), and Medical Physiology (HWB,KB), University of Groningen, Groningen, The Netherlands

Correspondence to: Jaap Oostendorp, Dept. of Molecular Pharmacology, University Centre for Pharmacy, University of Groningen, Antonius Deusinglaan 1, 9713 AV Groningen, The Netherlands. E-mail: j.oostendorp{at}farm.rug.nl

Various CC chemokine receptors are expressed on effector cells in allergic inflammation and their distinct expression pattern may dictate, to a large extent, the migration of inflammatory cells to sites of airway inflammation. The lipopolysaccharide (LPS)-inducible CC chemokine receptor (L-CCR) is an orphan chemokine receptor that has previously been identified in the murine macrophage cell line RAW 264.7 and in murine brain glial cells. In this study we investigated the induction and localization of L-CCR mRNA expression in mouse lung after ovalbumin (OVA)-induced airway inflammation. Both RT-PCR experiments and in situ hybridization (ISH) experiments in whole lung sections revealed a rapid upregulation of L-CCR mRNA expression as early as 1 hr and 3 hr after OVA challenge. Expression was found predominantly in MAC3⁺ macrophages and in bronchial epithelium, as shown by ISH and immunohistochemistry (IHC). We demonstrated that L-CCR mRNA expression is strongly upregulated in mouse lung after OVA challenge and is localized in macrophages and bronchial epithelium. Regarding the likely role of L-CCR as a chemokine receptor with the putative ligand monocyte chemotactic protein-1 (MCP-1, CCL2), this receptor may have an important function in the early phase of airway inflammation. (J Histochem Cytochem 52:401–410, 2004)

Key Words: mouse • ovalbumin challenge • L-CCR • macrophage • bronchial epithelium

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