Eosinophilic airway inflammation is the main histologic correlate of airway hyper-responsiveness (AHR) and tissue injury in the pathogenesis of bronchial asthma. There is strong evidence for a central role of CD4+ T-cells secreting pro-allergic Th2-cytokines, such as IL-4 and IL-5, in the induction of airway eosinophilia and AHR. IL-5 appears to be one of the main pro-inflammatory mediators among a growing number of cytokines and chemokines that induce, regulate and sustain eosinophilic airway inflammation. Animal studies provide confirmatory evidence for the important role of IL-5 in the induction and maintenance of eosinophilic airway infiltration leading to altered airway function. Interfering with the action of IL-5 represents one of the new immunomodulatory therapeutic strategies in the treatment of bronchial asthma. Compared to established immunosuppressive agents like steroids, a major advantage of this strategy is the specificity of reducing eosinophilic inflammation, thus possibly acting nearly without side effects. There are several possible ways to inhibit the effects of IL-5 including alteration of the signalling pathway in the IL-5 producing cell by inhibition or modification of transcription factors or the use of antisense oligonucleotides and blocking of the IL-5 protein itself by monoclonal antibodies, soluble IL-5 receptor or antagonists of the IL-5 receptor expressed on the surface of eosinophils. Although preliminary data from the first clinical trials gave rise to skepticism about the efficacy of anti-IL-5 treatment regarding the improvement of lung function of asthmatic patients, further studies with a better defined profile of the target population may provide encouraging results, allowing the introduction of this truly new therapeutic concept.