Interleukin-16 in a mouse model of allergic asthma

Abstract

Allergic asthma is a disease which affects an increasing number of people. Patients with this illness suffer from variable airflow obstruction and increased airway responsiveness to a variety of stimuli. Furthermore, an inflammatory response in the lungs occurs, accompanied by enhanced mucus production (10). In serum of these patients enhanced levels of IgE antibodies can be detected (reviewed in 238, 239). Currently, several different drugs are available for people who suffer from asthma. These medicines include corticosteroids, b2-agonists, leukotriene antagonists and phosphodiesterase inhibitors (240-244). Corticosteroids are the most effective and most used drug at this moment in the treatment of asthma to reduce the inflammatory component and hyperresponsiveness (245). However, corticosteroids are not very selective and affect a whole range of inflammatory and non-inflammatory cells (246-248). More importantly, all drugs that are available for people who suffer from allergic asthma do not cure these patients but only reduce the clinical symptoms of this disorder. Therefore, current research is focused on development of strategies that treat asthmatics at a more causal level of their illness.

It is now widely accepted that T-helper type 2 (Th2) lymphocytes play a causal role in allergic asthma (10, 249, 250). Th2 cells produce a limited set of cytokines including interleukin-3 (IL3), IL4, IL5, IL9, IL10 and IL13. Both in human asthmatic patients and murine models of allergic asthma Th2 subsets have been detected (8, 9) and it is extensively documented that the cytokines produced by these cells are crucial for development of allergic symptoms. New strategies could therefore be aimed at specifically targeting this T cell subset or the cytokines produced by these T cells (18, 251, 252).