1,721,227 research outputs found
Newer therapies for asthma: a focus on anti-IgE
No full textThe prevalence of asthma and other allergic disorders has been on the increase not only in the western world but also in the developing countries. This increasing prevalence has lead research into the discovery and development of various new therapeutic strategies. The improved understanding about the pathophysiology of asthma has prompted the developments of novel molecules to tackle this problem. These include newer phosphodiesterase inhibitors, cytokine modulation strategies, allergen immunotherapy, and anti-IgE. Immunoglobulin E plays a major role in airway inflammation in asthma. Omalizumab, a novel humanised monoclonal antibody directed against the high affinity FcepsilonRI portion of the IgE has shown a lot of promise in the control of asthma symptoms and as a steroid sparing agent in the management of allergic asthma. This new molecule has an excellent safety profile and could play an important role in the management of patients with severe asthma. This review gives a brief overview of the newer therapies under investigation with special reference to omalizumab in the treatment of allergic asthma
The Quintiles Prize Lecture 2004. the identification of the adenosine A2B receptor as a novel therapeutic target in asthma
No full textAdenosine is a powerful bronchoconstrictor of asthmatic, but not normal, airways. In vitro studies on isolated human mast cells and basophils revealed that adenosine and selective analogues augmented inflammatory mediator release from mast cells by stimulating A2 receptors. Pharmacological blockade of mast cell mediator release in vivo also attenuated adenosine-induced bronchoconstriction, as did theophylline, by adenosine A2 receptor antagonism. Further in vitro studies revealed that the asthmatic response to adenosine is likely to be mediated via the A2B subtype which is selectively antagonised by enprofylline. Studies in animal models, especially mice, have shown a close synergistic interaction between adenosine, Th2 and airway remodelling responses. The recent description of A2B receptors on human airway smooth muscle cells that mediate cytokine and chemokine release and induce differentiation of fibroblasts into myofibroblasts strengthens the view that adenosine maybe more than an inflammatory mediator in asthma but also participates in airway wall remodelling in this disease. These data have provided a firm basis for developing adenosine A2B receptor antagonists as a new therapeutic approach to this disease
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