The role of viruses in acute exacerbations of asthma

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Presentation transcript:

The role of viruses in acute exacerbations of asthma David J. Jackson, MD, Sebastian L. Johnston, MD, PhD Journal of Allergy and Clinical Immunology Volume 125, Issue 6, Pages 1178-1187 (June 2010) DOI: 10.1016/j.jaci.2010.04.021 Copyright © 2010 American Academy of Allergy, Asthma & Immunology Terms and Conditions

Fig 1 Epithelial and immune cell responses to rhinovirus infection. Following infection a wide range of mediators are secreted including pro-inflammatory cytokines, chemokines, interferons, and growth factors. This leads to eosinophilic, neutrophilic, and lymphocytic inflammation, as well as mucus hypersecretion and likely airway remodelling. CCL, CC chemokine ligand; CCL5, RANTES (Regulated on Activation Normal T-cell Expressed and Secreted); CCL11, eotaxin; CCL24, eotaxin-2; CXCL, CXC chemokine ligand; CXCL 1, GRO-α (growth-related oncogene α); CXCL-5, ENA-78 (epithelial neutrophil activating protein-78); CXCL10, IP-10 (IFN-γ-inducible protein 10); DC, dendritic cell; FGF-2, fibroblast growth factor-2; GMCSF, granulocyte macrophage-colony stimulating factor; ICAM-1, intercellular adhesion molecule-1; IFN, interferon; IL, interleukin; LDLR, low density lipoprotein receptor; RV, rhinovirus; TC1, cytotoxic CD8+ T lymphocyte type 1; TH1, T-helper 1 CD4+ T lymphocyte; TNF-α, tumour necrosis factor-α; VEGF, vascular endothelial growth factor. Journal of Allergy and Clinical Immunology 2010 125, 1178-1187DOI: (10.1016/j.jaci.2010.04.021) Copyright © 2010 American Academy of Allergy, Asthma & Immunology Terms and Conditions