Models of Exacerbations in Asthma and COPD (Contributions to by U. Sjöbring, J.D. Taylor, A. Schmidt, H. Herwald

By U. Sjöbring, J.D. Taylor, A. Schmidt, H. Herwald

This quantity offers an summary of exacerbation versions of bronchial asthma and protracted obstructive pulmonary ailment (COPD). inside of this broad box the booklet specializes in experimental structures that mimic pathobiological methods more likely to be severe in exacerbations of those stipulations. To generate perception into the mechanisms of exacerbation of pulmonary sickness and to advertise the invention of destiny remedies, either animal types and human experimental versions are defined. For this replace one of the most eminent scientists in the sector of pulmonology will be recruited to proportion their wisdom of this evolving box of human medication. versions of Exacerbations in bronchial asthma and COPD can be of serious curiosity to pulmonologists, allergologists, experts in inner medication and significant care, in addition to to microbiologists, infectiologists and pharmacologists learning the reaction to respiration infections.

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Additional resources for Models of Exacerbations in Asthma and COPD (Contributions to Microbiology)

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J Allergy Clin Immunol 1997;100:669–678. Robinson D, Hamid Q, Bentley A, Ying S, Kay AB, Durham SR: Activation of CD4ϩ T cells, increased TH2-type cytokine mRNA expression, and eosinophil recruitment in bronchoalveolar lavage after allergen inhalation challenge in patients with atopic asthma. J Allergy Clin Immunol 1993;92:313–324. Ali FR, Oldfield WL, Higashi N, Larche M, Kay AB: Late asthmatic reactions induced by inhalation of allergen-derived T cell peptides. Am J Respir Crit Care Med 2004;169:20–26.

After AIC, T lymphocytes have been shown to be clonally expanded in the lower respiratory tract, demonstrating the inhalation of sensitizing allergens can recruit allergen-specific T cell clones to the lung [24]. Furthermore, cytokines produced by activated Th2-type CD4ϩ T cells in the airway, such as IL-4 and IL-5, may contribute to late asthmatic responses by mechanisms that include eosinophil accumulation [25]. Following AIC, the development of late-phase asthmatic responses typically occur following IgE-mediated early-phase asthmatic responses.

3. Increasing concentrations of allergen inhaled into the airway may be required for the generation of the late-phase asthmatic response. low dose of inhaled antigen were found to be more likely to develop a late response, and it can be concluded that the occurrence of a late-phase asthmatic response probably depends on the dose of allergen administered but is independent of the degree of nonspecific bronchial responsiveness to methacholine prior to the challenge [30, 36]. Furthermore, when subjects are pretreated with antihistamine to allow a greater dose of inhaled allergen, it is possible to induce a late asthmatic response in subjects who previously demonstrated only an early response [37].

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