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

被引:17
作者
de Bie, JJ
Henricks, PAJ
Cruikshank, WW
Hofman, G
Nijkamp, FP
van Oosterhout, AJM
机构
[1] Univ Utrecht, Utrecht Inst Pharmaceut Sci, Dept Pharmacol & Pathobiol, NL-3508 TB Utrecht, Netherlands
[2] Boston Univ, Sch Med, Ctr Pulm, Boston, MA 02118 USA
关键词
eosinophil; hyperresponsiveness; asthma; interleukin-16 (murine);
D O I
10.1016/S0014-2999(99)00547-6
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
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. (C) 1999 Elsevier Science B.V. All rights reserved.
引用
收藏
页码:189 / 196
页数:8
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