In vivo relationship between collagenase-2 and interleukin-8 but not tumour necrosis factor-α in chronic rhinosinusitis with nasal polyposis

Katriina Kostamo, T. Sorsa, M. Leino, T. Tervahartiala, H. Alenius, M. Richardson, E. Toskala

    Research output: Contribution to journalArticlepeer-review

    Abstract

    Background: The characteristic feature of chronic rhinosinusitis with nasal polyposis (CRSwNP) is eosinophilic inflammation of the sinus mucosa; a type of inflammation also seen in asthmatic airways. Similar histopathologic findings of airway remodelling are present in both diseases. Remodelling is tightly controlled by matrix metalloproteinases (MMP). Increase of collagenase-2 (MMP-8) expression in the bronchial epithelial cells has been described in asthmatic patients, but it has not been studied in CRSwNP. Methods: The concentrations and degree of activation of MMP-8 were analysed by immunofluorometric assay and Western blotting, respectively, in sinus mucus samples from CRSwNP patients and in nasal lavages from healthy controls in relation to inductive cytokines interleukin-8 (IL-8) and tumour necrosis factor-α (TNF-α). Results: Significantly elevated levels of MMP-8 and IL-8 but not TNF-α were found in CRSwNP patients relative to controls. In particular, the activation of mesenchymal-type MMP-8 but not polymorphonuclear-type MMP-8 was associated with elevated IL-8 levels. Conclusions: The IL-8 and MMP-8 seemingly form an inductive cytokine-proteinase cascade in CRSwNP pathogenesis. Together they provide a target for novel therapies and a diagnostic tool for monitoring CRSwNP treatment. Copyright © Blackwell Munksgaard 2005.
    Original languageEnglish
    Pages (from-to)1275-1279
    Number of pages4
    JournalAllergy: European Journal of Allergy and Clinical Immunology
    Volume60
    Issue number10
    DOIs
    Publication statusPublished - Oct 2005

    Keywords

    • Chronic rhinosinusitis
    • Interleukin-8
    • Matrix metalloproteinase-8
    • Nasal polyposis
    • Tumour necrosis factor-α

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