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Exogenous interleukin‐16 inhibits antigen‐induced airway hyper‐reactivity, eosinophilia and Th2‐type cytokine production in mice
Author(s) -
De Bie J. J.,
Jonker E. H.,
Henricks P. A. J.,
Hoevenaars J.,
Little F. F.,
Cruikshank W. W.,
Nijkamp F. P.,
Van Oosterhout A. J. M.
Publication year - 2002
Publication title -
clinical and experimental allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.462
H-Index - 154
eISSN - 1365-2222
pISSN - 0954-7894
DOI - 10.1046/j.1365-2222.2002.01528.x
Subject(s) - ovalbumin , immunology , cytokine , immune system , antigen , bronchoalveolar lavage , interleukin 5 , eosinophilia , in vivo , interleukin , medicine , biology , lung , microbiology and biotechnology
Summary Background IL‐16 has been described as a natural soluble CD4‐ligand with immunosuppressive effects in vitro . However, little is known about the effect of IL‐16 on immune responses in vivo . Objective In the present study, we examined the effect of IL‐16 administration in a murine model of allergic asthma. Next, we determined whether these effects were mediated by modulation of CD4 + T lymphocytes. Methods and results Intraperitoneal administration of IL‐16 completely inhibits antigen‐induced airway hyper‐responsiveness and largely decreases the number of eosinophils in bronchoalveolar lavage fluid (> 90%) and airway tissue of ovalbumin‐sensitized and challenged mice. Firstly, it appears that thoracic lymph node cells isolated from in vivo IL‐16‐treated ovalbumin‐challenged animals produce less IL‐4 (77%) and IL‐5 (85%) upon antigenic re‐stimulation, when compared to vehicle‐treated mice. Secondly, pre‐incubation of lymphocytes with IL‐16 in vitro reduces antigen‐induced proliferation (55%) and Th2‐type cytokine production (IL‐4; 56%, IL‐5; 77%). Thirdly, the presence of IL‐16 during priming cultures of TCR transgenic T cells (DO11.10), reduces IL‐4 (33%) and IL‐5 (35%), but not IL‐10 and IFNγ levels upon re‐stimulation. Conclusion It can be concluded that IL‐16 has potent immunosuppressive effects on a Th2‐dominated allergic airway response.