SummaryInterlenkin 5 (IL-5) is the main factor that promotes the terminal differentiation of eosinophil progenitors (as indicated by colony formation assays), and enhances the effector capacity of mature eosinophils. IL-5 is produced by T lymphocytes, CD4-/CD8-and mast cells and recently, messenger (m)RNA of this cytokine has been identified in eosinophils from patients with coeliac disease, asthma, or eosinophilic heart diseases. In this study, IL-5 mRNA and immunoreactive IL-5 protein were detected in tissue and blood eosinophils from patients with eosinophilic cystitis or hypereosinophilic syndromes but not in Crohn's disease. By electron microscopy associated to immunogold staining, immunoreactive IL-5 was identified in eosinophilic granules. After stimulation with IgA-, IgE-, or IgG-immune complexes, blood eosinophils were shown, by immunocytochemistry and by enzyme-linked immunosorbent assay, to secrete IL-5. These observations demonstrate that eosinophils, under physiological stimulation, can release significant amounts of IL-5, which may contribute to local eosinophil recruitment and activation.

indicate a need for further rationalising the provision and distribution of special care baby units. The case for this is further strengthened by our other findings. Even in the three well-endowed regions in this study it has not proved possible to staff and equip all officially recognised units to the standard recommended by the expert group. Moreover, since the group's report was published, increasing technological requirements together with inflation have made it a continuing struggle to maintain the standard of excellence required of the few units that provide intensive care for the illest babies. A further argument for rationalisation is the demonstration by Blake et a19 of the successful results of transporting sick babies when this is well organised by the intensive care nursery that is to receive the babies. Any replanning of nurseries must, however, take into account References

The in vivo inhibitory effect of a new antiallergic, anti-H1 drug, cetirizine, on eosinophil attraction at skin sites challenged with various stimuli has been recently suggested. In the present work, we confirmed that this molecule, at therapeutical concentration, has a potent inhibitory action on eosinophil response to different chemoattractant mediators such as platelet-activating factor (PAF acether) and N-formyl methionyl leucyl phenyl alanyl in vitro. Another anti-H1 drug, polaramine, did not show this effect at the same concentration. These findings suggest that cetirizine in addition to its antihistaminic effect could also play a direct inhibitory effect on eosinophil recruitment. Moreover, cetirizine was not toxic for eosinophils and did not induce degranulation, as shown by the absence of peroxidase release. Comparison between cetirizine and a PAF acether antagonist (BN 52021) suggested that cetirizine did not act by a PAF receptor-blocking activity.