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Enhanced airway inflammation and decreased subepithelial fibrosis in interleukin 6-deficient mice following chronic exposure to aerosolized antigen.
Clin Exp Allergy. 2004 Aug; 34(8):1321-8.CE

Abstract

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-beta1 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.

Authors+Show Affiliations

Respiratory Medicine, Cellular Transplantation Biology, Kanazawa Graduate University School of Medicine, Kanazawa, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

15298576

Citation

Qiu, Z, et al. "Enhanced Airway Inflammation and Decreased Subepithelial Fibrosis in Interleukin 6-deficient Mice Following Chronic Exposure to Aerosolized Antigen." Clinical and Experimental Allergy : Journal of the British Society for Allergy and Clinical Immunology, vol. 34, no. 8, 2004, pp. 1321-8.
Qiu Z, Fujimura M, Kurashima K, et al. Enhanced airway inflammation and decreased subepithelial fibrosis in interleukin 6-deficient mice following chronic exposure to aerosolized antigen. Clin Exp Allergy. 2004;34(8):1321-8.
Qiu, Z., Fujimura, M., Kurashima, K., Nakao, S., & Mukaida, N. (2004). Enhanced airway inflammation and decreased subepithelial fibrosis in interleukin 6-deficient mice following chronic exposure to aerosolized antigen. Clinical and Experimental Allergy : Journal of the British Society for Allergy and Clinical Immunology, 34(8), 1321-8.
Qiu Z, et al. Enhanced Airway Inflammation and Decreased Subepithelial Fibrosis in Interleukin 6-deficient Mice Following Chronic Exposure to Aerosolized Antigen. Clin Exp Allergy. 2004;34(8):1321-8. PubMed PMID: 15298576.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Enhanced airway inflammation and decreased subepithelial fibrosis in interleukin 6-deficient mice following chronic exposure to aerosolized antigen. AU - Qiu,Z, AU - Fujimura,M, AU - Kurashima,K, AU - Nakao,S, AU - Mukaida,N, PY - 2004/8/10/pubmed PY - 2004/12/21/medline PY - 2004/8/10/entrez SP - 1321 EP - 8 JF - Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology JO - Clin Exp Allergy VL - 34 IS - 8 N2 - 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-beta1 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. SN - 0954-7894 UR - https://www.unboundmedicine.com/medline/citation/15298576/Enhanced_airway_inflammation_and_decreased_subepithelial_fibrosis_in_interleukin_6_deficient_mice_following_chronic_exposure_to_aerosolized_antigen_ DB - PRIME DP - Unbound Medicine ER -