By U. Sjöbring, J.D. Taylor, A. Schmidt, H. Herwald
Exacerbations of bronchial asthma and COPD: definitions, scientific manifestations and epidemiology / O'Byrne, P.M. -- Human rhinovirus types 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 apartment dirt mite publicity / Cates, E.C. ... [et al.] --, respiration syncytial virus-induced pulmonary ailment and exacerbation of allergic bronchial asthma / Lukacs, N.W. ... [et al.] -- Lipopolysaccharide problem of people as a version for power obstructive lung sickness exacerbations / Kharitonov, S.A.; Sjobring, U. -- A human rhinovirus version of power obstructive pulmonary sickness exacerbations / Contoli, M. ... [et al.] -- Animal versions of cigarette smoke-induced power obstructive lung disorder / Churg, A.; Wright, J.L. -- Animal versions of persistent obstructive pulmonary affliction exacerbations / Gaschler, G.J. ... [et al.]
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Interactions between leukocytes, tissue and cell mediators. Allergen cross-links IgE receptors on mast cells and basophils, inducing release of pre-formed and newly synthesized mediators. Dendritic cells capture antigen and present to T lymphocytes, which clonally expand and release Th2 cytokines. Eosinophils and basophils are activated by cytokines such as IL-5 and attracted by chemokines such as eotaxin. ECP ϭ Eosinophilic cationic protein. Mechanisms of the Late-Phase Asthmatic Response During the late-phase asthmatic response, mediators thought to originate from mast cells can also be measured at levels similar to those observed during the early-phase response [11, 15].
The major obstacle to the development of mouse models is the host cell tropism of RV. Approximately 10% of RV serotypes can use both the human and mouse forms of low-density lipoprotein receptor, and a mouse model capitalizing on this fact was established [4]. However, the remaining 90% of RV use human Xatzipsalti/Papadopoulos 34 ICAM-1 to attach and enter the cells. These viruses do not bind to mouse ICAM-1 and therefore infection of mice or of mouse bronchial epithelial cells with the major RV variants is not possible.
In order to model such a response, peripheral blood mononuclear cells (PBMC) have been used. PBMC were infected with RV leading to an increase in the expression of the early activation marker CD69 on T cells. RV also induced the secretion of IFN-␥ from both peripheral blood T cells and NK cells [20], as well as the production of IL-8 [21]. Exposure of PBMC from normal and atopic asthmatic subjects to RV resulted in an upregulation of IFN-␥, IL-12, and IL-10 production in both groups although the IFN-␥ response was considerably lower in asthmatics [22].