Nakajima H, Iwamoto I, Yoshida S
Second Department of Internal Medicine, Chiba University School of Medicine, Japan.
Am Rev Respir Dis. 1993 Oct;148(4 Pt 1):1102-4. doi: 10.1164/ajrccm/148.4_Pt_1.1102.
In a murine model of airway late-phase reaction we have previously shown that antigen-induced eosinophil recruitment into the airways of sensitized mice is mediated by CD4+ T cells and interleukin-5. To determine whether interferon-gamma (IFN-gamma) regulates antigen-induced eosinophil recruitment into the airways, we studied the effect of aerosolized recombinant murine IFN-gamma on the eosinophil infiltration of the trachea induced by antigen inhalation in mice. The administration of aerosolized rIFN-gamma prevented antigen-induced eosinophil infiltration in the trachea of sensitized mice. The administration of aerosolized rIFN-gamma also decreased antigen-induced CD4+ but not CD8+ T-cell infiltration in the trachea. However, there were no significant changes in the number of blood eosinophils or of splenic CD4+ and CD8+ T cells in the treatment with rIFN-gamma. These results indicate that locally administered IFN-gamma prevents antigen-induced eosinophil recruitment into the airways by inhibiting CD4+ T cell infiltration.
在气道迟发相反应的小鼠模型中，我们之前已表明，抗原诱导的嗜酸性粒细胞募集至致敏小鼠气道是由CD4 + T细胞和白细胞介素-5介导的。为了确定干扰素-γ（IFN-γ）是否调节抗原诱导的嗜酸性粒细胞募集至气道，我们研究了雾化重组鼠IFN-γ对小鼠吸入抗原诱导的气管嗜酸性粒细胞浸润的影响。雾化rIFN-γ的给药可防止致敏小鼠气管中抗原诱导的嗜酸性粒细胞浸润。雾化rIFN-γ的给药还可减少抗原诱导的气管中CD4 +而非CD8 + T细胞浸润。然而，rIFN-γ治疗组的血液嗜酸性粒细胞数量以及脾脏CD4 +和CD8 + T细胞数量均无显著变化。这些结果表明，局部给予IFN-γ可通过抑制CD4 + T细胞浸润来防止抗原诱导的嗜酸性粒细胞募集至气道。
