By U. Sjöbring, J.D. Taylor, A. Schmidt, H. Herwald
Exacerbations of bronchial asthma and COPD: definitions, medical manifestations and epidemiology / O'Byrne, P.M. -- Human rhinovirus versions in bronchial asthma / Singh, A.M.; Busse, W.W. -- Allergen inhalation problem: a human version of bronchial asthma exacerbation / Gauvreau, G.M.; Evans, M.Y. -- mobile and animals versions for rhinovirus an infection in bronchial asthma / Xatzipsalti, M.; Papadopoulos, N.G. -- Modeling responses to respiration condo dirt mite publicity / Cates, E.C. ... [et al.] --, breathing syncytial virus-induced pulmonary illness and exacerbation of allergic bronchial asthma / Lukacs, N.W. ... [et al.] -- Lipopolysaccharide problem of people as a version for continual obstructive lung ailment exacerbations / Kharitonov, S.A.; Sjobring, U. -- A human rhinovirus version of persistent obstructive pulmonary disorder exacerbations / Contoli, M. ... [et al.] -- Animal versions of cigarette smoke-induced continual obstructive lung affliction / Churg, A.; Wright, J.L. -- Animal types of power obstructive pulmonary sickness exacerbations / Gaschler, G.J. ... [et al.]
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Extra resources for Models of Exacerbations in Asthma and COPD
Example text
Oddera S, Silvestri M, Penna R, Galeazzi G, Crimi E, Rossi GA: Airway eosinophilic inflammation and bronchial hyperresponsiveness after allergen inhalation challenge in asthma. Lung 1998;176:237–247. MacIntyre D, Boyd G: Factors influencing the occurrence of a late reaction to allergen challenge in atopic asthmatics. Clin Allergy 1984;14:311–317. Matsumoto K, Gauvreau GM, Rerecich T, Watson RM, Wood LJ, O’Byrne PM: IL-10 production in circulating T cells differs between allergen-induced isolated early and dual asthmatic responders.
Although the bronchial epithelium forms a barrier between the airway lumen and the underlying cells and is actively involved in the immune response to RV through the production of a variety of immunomodulatory factors, nonepithelial cells of mesenchymal origin may also play a major role. The presence of RV has been detected in subepithelial cells by in situ hybridization, suggesting that the virus could spread to fibroblasts via infected epithelial cells and therefore these cells may participate in the inflammatory response.
However, OVA preparations and HDM are two vastly different materials. This chapter is specifically concerned with modeling responses to HDM exposure in mice. These studies have furnished new information and unlocked new lines of inquiry regarding biological responses to common aeroallergens. The complexity of HDM as an allergen source, with its plethora of protein and nonprotein immunogenic components, may influence the mechanisms underlying sensitization, inflammation and remodeling. Here, we will discuss this issue, along with giving critical thought to the use of experimental models.
