Chlamydophila pneumoniae in human immortal Jurkat cells and primary lymphocytes uncontrolled by interferon-¦Ã

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• 作者：Kasumi Ishida^a ; Takeru Kubo^a ; Ayumi Saeki^b ; Chikayo Yamane^a ; Junji Matsuo^a ; Yimin^c ; Shinji Nakamura^d ; Yasuhiro Hayashi^a ; Miyuki Kunichika^d ; Mitsutaka Yoshida^e ; Kaori Takahashi^e ; Itaru Hirai^f ; Yoshimasa Yamamoto^f ; ^g ; Ken-ichiro Shibata^b ; Hiroyuki Yamaguchi^a ; ^{hiroyuki@med.hokudai.ac.jp}
• 关键词：Chlamydophila pneumoniae ; Indoleamine 2 ; 3-dioxygenase ; Interferon-¦Ã ; Lymphocytes
• 刊名：Microbes and Infection
• 出版年：2013
• 出版时间：March, 2013
• 年：2013
• 卷：15
• 期：3
• 页码：192-200
• 全文大小：806 K

文摘

Lymphocytes are a potential host cell for Chlamydophila pneumoniae, although why the bacteria must hide in lymphocytes remains unknown. Meanwhile, interferon (IFN)-¦Ã 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-¦Ã. C. pneumoniae grew normally in human lymphoid Jurkat cells, even in the presence of IFN-¦Ã or under stimulation with phorbol myristate acetate plus ionomycin. Although Jurkat cells expressed IFN-¦Ã 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-¦Ã. Furthermore, C. pneumoniae in spleen cells obtained from IFN-¦Ã knockout mice with C57BL/6 background was maintained in a similar way to wild-type mice, supporting a minimal role of IFN-¦Ã-related response for eliminating C. pneumoniae from lymphocytes. Thus, we concluded that IFN-¦Ã 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.