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Effect of interleukin-16-blocking peptide on parameters of allergic asthma in a murine model.

Authors: De Bie, JJ  Henricks, PA  Cruikshank, WW  Hofman, G  Nijkamp, FP  Van Oosterhout, AJ 
Citation: de Bie JJ, etal., Eur J Pharmacol. 1999 Oct 27;383(2):189-96.
Pubmed: (View Article at PubMed) PMID:10585533

In this study, we examined whether peptides based on the hydrophilic Cluster of Differentiation (CD) 4-binding part of the amino acid sequence of human interleukin-16 can block interleukin-16-induced chemotaxis of murine lymphocytes in vitro. Peptide 3 was capable of inhibiting interleukin-16-induced chemotaxis of murine splenocytes in vitro. Next, we compared the effects of intra-airway administration of peptide 3 with those of antibodies to interleukin-16 on antigen-induced features in a murine model of allergic asthma. Intra-airway administration of peptide 3 largely inhibited the development of antigen-induced airway hyperresponsiveness while airway eosinophilia was not affected. Similar effects were observed after intranasal application of antibodies to interleukin-16. These results indicate that treatment with peptide 3 causes the same effects as do antibodies to interleukin-16, possibly via the inhibition of interaction between interleukin-16 and its receptor CD4. Therefore, peptide 3 could be useful as a lead compound in attempting to limit airway hyperresponsiveness via binding to CD4.


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CRRD Object Information
CRRD ID: 5024937
Created: 2011-03-02
Species: All species
Last Modified: 2011-03-02
Status: ACTIVE


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