[Immunopathogenesis of bronchial asthma]

Allergic asthma is a chronic pulmonary disease associated with bronchoconstriction and inflammation. Recent studies have shown that mediator substances and proinflammatory cytokines produced by mast cells, eosinophils and T-lymphocytes appear to be important for the pathogenesis of asthma. These substances contribute both to the initiation and perpetuation of the disease. In particular, it has been shown that allergic asthma is associated with increased TH2 (IL-4, IL-5, IL-13) cytokine production that causes activation of eosinophils and T-cells and production of chemokines (e.g. eotaxin) by pulmonary fibroblasts. Based on recent advances in our understanding of the immunopathogenesis of asthma in animal models several novel therapeutic approaches have been developed. Such approaches comprise treatment with recombinant anti-inflammatory cytokines, treatment with TH1-inducing cytokines such as IL-12, induction of oral tolerance and TGF-beta producing T-cells that can provide bystander suppression for TH2 cells, inhibitors of IgE, and antagonists of proinflammatory cytokines (e.g. IL-4 and IL-5) and their receptors. These novel treatment modalities will hopefully permit a more selective and effective suppression of pulmonary inflammation and bronchoconstriction in patients with allergic asthma compared to local treatment with corticosteroids. However, the clinical value of these novel therapeutic approaches remains to be determined. In particular, long term efficacy and safety of immunomodulatory therapy has to be studied more in detail.