A critical role for mouse CXC chemokine(s) in pulmonary neutrophilia during th type 1-dependent airway inflammation
A critical role for mouse CXC chemokine(s) in pulmonary neutrophilia during th type 1-dependent airway inflammation
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DOI：
10.4049/jimmunol.167.4.2349
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发表时间：
2001-08-15
影响因子：
4.4
通讯作者：
Nishimura, T
中科院分区：
文献类型：
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作者：
Takaoka, A;Tanaka, Y;Nishimura, T
抗原特异性的Th1和Th2细胞已被证明在诱发变态反应性疾病中发挥关键作用。在这里，我们研究了Th1诱导的呼吸道炎症的确切机制。通过转移新鲜诱导的OVA特异性Th1或Th2细胞，然后吸入OVA，诱导BALB/c小鼠呼吸道炎症。在该模型中，Th1和Th2细胞均可诱导呼吸道炎症。前者引起呼吸道中性粒细胞增多，而后者引起嗜酸性粒细胞增多。此外，我们发现Th1细胞比Th2细胞诱导更严重的气道高反应性(AHR)。抗IL-5单抗可几乎完全阻断Th2细胞输注所致的嗜酸性粒细胞增多，但抗IL-4单抗不能完全阻断Th2细胞输注诱导的嗜酸性粒细胞增多症。反之，抗人IL-8R单抗可抑制Th1诱导的AHR和肺中性粒细胞增多，阻断小鼠CXC趋化因子(S)的功能。这些发现揭示了小鼠CXC趋化因子(S)在Th1依赖性肺中性粒细胞增多和AHR中的关键作用。
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.