Endogenous IL-18 in experimentally induced asthma affects cytokine serum levels but is irrelevant for clinical symptoms

被引:23
作者
Hartwig, Christina
Tschernig, Thomas
Mazzega, Miriam
Braun, Armin [2 ]
Neumann, Detlef [1 ]
机构
[1] Hannover Med Sch, Inst Pharmacol OE 5320, D-30625 Hannover, Germany
[2] Fraunhofer Inst Toxicol & Expt Med, Dept Immunol Allergol & Clin Inhalat, Hannover, Germany
关键词
IL-18; asthma; ovalbumin; cytokines; mouse;
D O I
10.1016/j.cyto.2008.02.012
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
T cells and T cell derived cytokines are involved in the complex pathogenesis of asthma. The role of the cytokine IL-18 however, is not clearly defined so far. On the one hand side IL-18 induces Th1-type cytokines and thereby might counter-regulate Th2-mediated allergic asthma. On the other hand IL-18 also bears pro-inflammatory effects possibly enhancing experimental asthma. In order to elucidate the role of IL-18 in allergic pulmonary inflammation typical symptoms were compared after induction of experimental asthma in IL-18(-/-) and in wild type mice. Asthma was induced using ovalbumin (OVA) as allergen for sensitization and challenge. Sham sensitized and OVA challenged mice served as controls. Bronchoalveolar lavage-fluid cytology, leukocyte infiltration in lung tissues, serum levels of OVA-specific IgE and cytokines, and lung function were analyzed. Clear differences could be observed between control and asthmatic mice, both in wild type and IL-18(-/-) animals. Surprisingly, no differences were found between asthmatic wild type and IL-18(-/-) mice. Thus, in contrast to conflicting data in the literature IL-18 did not suppress or enhance the pulmonary allergic immune response in a murine experimental model of asthma. (C) 2008 Elsevier Ltd. All rights reserved.
引用
收藏
页码:298 / 305
页数:8
相关论文
共 25 条
[1]   Differential roles of IL-18 in allergic airway disease: Induction of eotaxin by resident cell populations exacerbates eosinophil accumulation [J].
Campbell, E ;
Kunkel, SL ;
Strieter, RM ;
Lukacs, NW .
JOURNAL OF IMMUNOLOGY, 2000, 164 (02) :1096-1102
[2]  
Campbell EM, 2000, METH MOL B, V138, P295
[3]  
Dinarello CA, 1997, J BIOL REG HOMEOS AG, V11, P91
[4]   IL-18:: A TH1-inducing, proinflammatory cytokine and new member of the IL-1 family [J].
Dinarello, CA .
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, 1999, 103 (01) :11-24
[5]   Interleukin-1β, interleukin-18, and the interleukin-1β converting enzyme [J].
Dinarello, CA .
MOLECULAR MECHANISMS OF FEVER, 1998, 856 :1-11
[6]   Interleukin 5 deficiency abolishes eosinophilia, airways hyperreactivity, and lung damage in a mouse asthma model [J].
Foster, PS ;
Hogan, SP ;
Ramsay, AJ ;
Matthaei, KI ;
Young, IG .
JOURNAL OF EXPERIMENTAL MEDICINE, 1996, 183 (01) :195-201
[7]   T-bet inhibits both TH2 cell-mediated eosinophil recruitment and TH17 cell-mediated neutrophil recruitment into the airways [J].
Fujiwara, Michio ;
Hirose, Koichi ;
Kagami, Shin-ichiro ;
Takatori, Hiroaki ;
Wakashin, Hidefumi ;
Tamachi, Tomohiro ;
Watanabe, Norihiko ;
Saito, Yasushi ;
Iwamoto, Itsuo ;
Nakajima, Hiroshi .
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, 2007, 119 (03) :662-670
[8]   Invasive versus noninvasive measurement of allergic and cholinergic airway responsiveness in mice [J].
Glaab, T ;
Ziegert, M ;
Baelder, R ;
Korolewitz, R ;
Braun, A ;
Hohlfeld, JM ;
Mitzner, W ;
Krug, N ;
Hoymann, HG .
RESPIRATORY RESEARCH, 2005, 6 (1)
[9]  
Hayashi N, 2007, P NATL ACAD SCI USA, V104, P14765, DOI 10.1073/pnas.0706378104
[10]  
Herz U, 1998, CLIN EXP ALLERGY, V28, P625