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Publisher Summary Asthma has been characterized as a disease associated with chronic inflammation, which may underlie the prevalent bronchial hyperresponsiveness in asthmatics. Antagonism of intercellular adhesion molecule 1 (ICAM-1) is a novel therapeutic approach to reduce the airway hyperresponsiveness. A soluble form of ICAM-1, which is normally membrane bound, potently inhibits human rhinovirus infection. Neural control of the airway caliber and the indirect effects of neurotransmitters, contributing to airway inflammation, continue to be investigated. Important advances in the understanding of the role of peptides, adrenergic receptors, and muscarinic receptors and autoreceptors in the airways have been made. Overexpression of a human chimeric α subunit of the high affinity IgE receptor (FcERI) has presented the opportunity for identifying specific antagonists of the IgE/FcERI binding interaction, which may prove to be effective in the treatment of allergic diseases. This chapter discusses the regulators of lipid mediators, such as leukotriene antagonists and 5-lipoxygenase inhibitors, as well as inhaled β-agonists. Those agonists are effective bronchodilators and have achieved wide therapeutic use against asthma. |