IngentaConnect Enhanced airway inflammation and decreased subepithelial fibrosis...

Authors: Z. Qiu; M. Fujimura¹; K. Kurashima¹; S. Nakao¹; N. Mukaida²

Source: Clinical & Experimental Allergy, Volume 34, Number 8, August 2004 , pp. 1321-1328(8)

Abstract:

Summary Background

Airway inflammation and remodelling are characteristic features of chronic asthma. Objective

To elucidate the role of interleukin (IL)-6 in airway responses to chronic antigen exposure. Methods

We compared airway inflammation, subepithelial collagen deposition, cytokine mRNA expression, and airway responsiveness between IL-6-deficient and wild-type (WT) mice following sensitization and repeated exposure to ovalbumin (OVA) three times a week for 8 weeks. Results

The repeated exposure to OVA induced infiltration of eosinophils, neutrophils, and lymphocytes into the airway, and caused thickening of the basement membrane and subepithelial fibrosis. IL-6-deficient mice exhibited more pronounced infiltration of these cells, a thinner basement membrane, and decreased subepithelial fibrosis, compared with WT mice. The repeated OVA exposure increased expression of IL-4, IL-13, eotaxin, monocyte chemoattractant protein-1 (MCP-1), and transforming growth factor- beta

1 mRNA in WT mice. Among these factors, expression of IL-13 and MCP-1 mRNA was further enhanced in IL-6-deficient mice, compared with WT mice. However, both WT and IL-6-deficient mice exhibited similar levels of airway responsiveness to increasing doses of methacholine, even after repeated exposure to OVA. Conclusion

These results suggest that IL-6 has dual roles in the chronic phase of asthma: down-regulation of inflammatory cell infiltration and enhancement of airway remodelling.

Keywords: airway hyper-responsiveness; airway inflammation; airway remodelling; chemokines; chronic antigen exposure; cytokines; IL-6-deficient mice

Document Type: Research article

DOI: 10.1111/j.1365-2222.2004.02013.x

Affiliations: 1: Respiratory Medicine, Cellular Transplantation Biology, Kanazawa Graduate University School of Medicine, Kanazawa, Japan, 2: Division of Molecular Bioregulation, Cancer Research Institute, Kanazawa University, Kanazawa, Japan

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Enhanced airway inflammation and decreased subepithelial fibrosis in interleukin 6-deficient mice following chronic exposure to aerosolized antigen