Department of Medical Laboratory Science, Faculty of Health Sciences, Hokkaido University, Nishi-5 Kita-12 Jo, Kita-ku, Sapporo, Hokkaido 060-0812, Japan.
Microbes Infect. 2013 Mar;15(3):192-200. doi: 10.1016/j.micinf.2012.11.006. Epub 2012 Nov 20.
Lymphocytes are a potential host cell for Chlamydophila pneumoniae, although why the bacteria must hide in lymphocytes remains unknown. Meanwhile, interferon (IFN)-γ is a crucial factor for eliminating chlamydiae from infected cells through indoleamine 2,3-dioxygenase (IDO) expression, resulting in depletion of tryptophan. We therefore assessed if lymphocytes could work as a shelter for the bacteria to escape IFN-γ. C. pneumoniae grew normally in human lymphoid Jurkat cells, even in the presence of IFN-γ or under stimulation with phorbol myristate acetate plus ionomycin. Although Jurkat cells expressed IFN-γ receptor CD119, their lack of IDO expression was confirmed by RT-PCR and western blotting. Also, C. pneumoniae survived in enriched human peripheral blood lymphocytes, even in the presence of IFN-γ. Furthermore, C. pneumoniae in spleen cells obtained from IFN-γ knockout mice with C57BL/6 background was maintained in a similar way to wild-type mice, supporting a minimal role of IFN-γ-related response for eliminating C. pneumoniae from lymphocytes. Thus, we concluded that IFN-γ did not remove C. pneumoniae from lymphocytes, possibly providing a shelter for C. pneumoniae to escape from the innate immune response, which has direct clinical significance.
淋巴细胞是肺炎衣原体的潜在宿主细胞，但细菌为何必须藏身于淋巴细胞中仍不得而知。同时，干扰素 (IFN)-γ 通过吲哚胺 2,3-双加氧酶 (IDO) 的表达，是从感染细胞中清除衣原体的关键因素，导致色氨酸耗竭。因此，我们评估了淋巴细胞是否可以作为细菌的避难所，以逃避 IFN-γ。肺炎衣原体在人淋巴样 Jurkat 细胞中正常生长，即使存在 IFN-γ 或佛波醇肉豆蔻酸乙酸酯加离子霉素刺激时也是如此。尽管 Jurkat 细胞表达 IFN-γ 受体 CD119，但通过 RT-PCR 和 Western blot 证实它们缺乏 IDO 表达。此外，即使存在 IFN-γ，富含人外周血淋巴细胞中的肺炎衣原体也能存活。此外，从 IFN-γ 敲除小鼠（C57BL/6 背景）获得的脾细胞中的肺炎衣原体也以类似方式维持，这支持 IFN-γ 相关反应在从淋巴细胞中消除肺炎衣原体方面的作用最小。因此，我们得出结论，IFN-γ 并未从淋巴细胞中清除肺炎衣原体，这可能为肺炎衣原体逃避先天免疫反应提供了庇护所，这具有直接的临床意义。
