| Title: | Chlamydophila pneumoniae in human immortal Jurkat cells and primary lymphocytes uncontrolled by interferon-γ |
| Authors: | Ishida, Kasumi Browse this author |
| Kubo, Takeru Browse this author |
| Saeki, Ayumi Browse this author →KAKEN DB |
| Yamane, Chikayo Browse this author |
| Matsuo, Junji Browse this author →KAKEN DB |
| Yimin Browse this author →KAKEN DB |
| Nakamura, Shinji Browse this author →KAKEN DB |
| Hayashi, Yasuhiro Browse this author →KAKEN DB |
| Kunichika, Miyuki Browse this author |
| Yoshida, Mitsutaka Browse this author |
| Takahashi, Kaori Browse this author |
| Hirai, Itaru Browse this author |
| Yamamoto, Yoshimasa Browse this author |
| Shibata, Ken-Ichiro Browse this author →KAKEN DB |
| Yamaguchi, Hiroyuki Browse this author →KAKEN DB |
| Keywords: | Chlamydophila pneumoniae |
| Indoleamine 2,3-dioxygenase |
| Interferon-γ |
| Lymphocytes |
| Issue Date: | Mar-2013 |
| Journal Title: | Microbes and infection / Institut Pasteur |
| Volume: | 15 |
| Issue: | 3 |
| Start Page: | 192 |
| End Page: | 200 |
| Publisher DOI: | 10.1016/j.micinf.2012.11.006 |
| PMID: | 23178757 |
| Abstract: | 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. |
| Type: | article (author version) |
| URI: | http://hdl.handle.net/2115/52246 |
| Appears in Collections: | 保健科学院・保健科学研究院 (Graduate School of Health Sciences / Faculty of Health Sciences) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)
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