Effect of interleukin-16-blocking peptide on parameters of allergic asthmain a murine model

In this study, we examined whether peptides based on the hydrophilic Cluste r of Differentiation (CD) 4-binding part of the amino acid sequence of huma n interleukin-16 can block interleukin-16-induced chemotaxis of murine lymp hocytes in vitro. Peptide 3 was capable of inhibiting interleukin-16-induce d chemotaxis of murine splenocytes in vitro. Next, we compared the effects of intra-airway administration of peptide 3 with those of antibodies to int erleukin-16 on antigen-induced features in a murine model of allergic asthm a. Intra-airway administration of peptide 3 largely inhibited the developme nt of antigen-induced airway hyperresponsiveness while airway eosinophilia was not affected. Similar effects were observed after intranasal applicatio n of antibodies to interleukin-16. These results indicate that treatment wi th peptide 3 causes the same effects as do antibodies to interleukin-16, po ssibly via the inhibition of interaction between interleukin-16 and its rec eptor CD4. Therefore, peptide 3 could be useful as a lead compound in attem pting to limit airway hyperresponsiveness via binding to CD4. (C) 1999 Else vier Science B.V. All rights reserved.