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Asthma is a chronic respiratory disease characterized by bronchial hyperreactivity. There are several endotypes of which allergic asthma is the most common. Severe eosinophilic asthma is prevalent in approximately 5% of asthmatics and its phenotype overlaps with allergic asthma and type 2 inflammation. Patients with refractiveness to corticosteroids underline the difficulty in controlling persistent inflammation in severe eosinophilic asthma. The focus of biological therapies is geared towards the understanding of the intricate interplay of the cytokines that drive the eosinophil’s ability to induce chronic inflammation with airway obstruction. This chapter takes the reader down a historical journey of initial studies that were performed using mouse helper T cell clones for reconstitution experiments to unravel the mechanism of the role T helper 2 cytokines play in allergic asthma. We then reviewed the classic in vivo experiments that demonstrated how antibodies to IL5 can down regulate eosinophils in the blood and their progenitors in the bone marrow of mice. We also delve into the complex interaction of the alarmins on the cytokines triggers of allergic inflammation with elevated eosinophils. Finally, we review the clinical literature on the beneficial effects of humanized monoclonal antibodies in use for treatment of patients suffering from severe eosinophilic asthma.