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The Journal of Immunology, 2001, 167: 2349-2353.
Copyright © 2001 by The American Association of Immunologists

A Critical Role for Mouse CXC Chemokine(s) in Pulmonary Neutrophilia During Th Type 1-Dependent Airway Inflammation1

Akiko Takaoka*, Yoshitaka Tanaka*, Takemasa Tsuji{dagger}, Takafumi Jinushi{dagger}, Akihiko Hoshino*, Yumiko Asakura*, Yasuo Mita*, Kazuhito Watanabe*, Shiro Nakaike*, Yuji Togashi{dagger}, Toshiaki Koda{dagger}, Kouji Matsushima{ddagger} and Takashi Nishimura2,{dagger}

* Medicinal Research Laboratory, Taisho Pharmaceutical, Saitama, Japan; {dagger} Division of Immunoregulation, Institute for Genetic Medicine, Hokkaido University, Sapporo, Japan; and {ddagger} Department of Molecular Preventive Medicine, University of Tokyo, Tokyo, Japan

Ag-specific Th1 and Th2 cells have been demonstrated to play a critical role in the induction of allergic diseases. Here we have investigated the precise mechanisms of Th1-induced airway inflammation. Airway inflammation was induced in BALB/c mice by transfer of freshly induced OVA-specific Th1 or Th2 cells followed by OVA inhalation. In this model, both Th1 and Th2 cells induced airway inflammation. The former induced neutrophilia in airways, whereas the latter induced eosinophilia. Moreover, we found that Th1 cells induced more severe airway hyperresponsiveness (AHR) than Th2 cells. The eosinophilia induced by Th2 cell infusion was almost completely blocked by administration of anti-IL-5 mAb, but not anti-IL-4 mAb. In contrast, Th1-induced AHR and pulmonary neutrophilia were inhibited by the administration of anti-human IL-8R Ab, which blocks the function of mouse CXC chemokine(s). These findings reveal a critical role of mouse CXC chemokine(s) in Th1-dependent pulmonary neutrophilia and AHR.




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