title: Chlamydophila pneumoniae in human immortal Jurkat cells and primary lymphocytes uncontrolled by interferon-γ.
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.
authors.affiliation: Department of Medical Laboratory Science, Faculty of Health Sciences, Hokkaido University, Nishi-5 Kita-12 Jo, Kita-ku, Sapporo, Hokkaido 060-0812, Japan.
authors.forename: Kasumi
authors.initials: K
authors.lastname: Ishida
authors.forename: Takeru
authors.initials: T
authors.lastname: Kubo
authors.forename: Ayumi
authors.initials: A
authors.lastname: Saeki
authors.forename: Chikayo
authors.initials: C
authors.lastname: Yamane
authors.forename: Junji
authors.initials: J
authors.lastname: Matsuo
authors.lastname: Yimin
authors.forename: Shinji
authors.initials: S
authors.lastname: Nakamura
authors.forename: Yasuhiro
authors.initials: Y
authors.lastname: Hayashi
authors.forename: Miyuki
authors.initials: M
authors.lastname: Kunichika
authors.forename: Mitsutaka
authors.initials: M
authors.lastname: Yoshida
authors.forename: Kaori
authors.initials: K
authors.lastname: Takahashi
authors.forename: Itaru
authors.initials: I
authors.lastname: Hirai
authors.forename: Yoshimasa
authors.initials: Y
authors.lastname: Yamamoto
authors.forename: Ken-ichiro
authors.initials: K
authors.lastname: Shibata
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Yamaguchi
mesh_terms: D000818:Animals; D023521:Chlamydophila Infections / Q000276:immunology / Q000382:microbiology; D016993:Chlamydophila pneumoniae / Q000187:drug effects / Q000276:immunology*; D005260:Female; D006367:HeLa Cells; D006801:Humans; D050503:Indoleamine-Pyrrole 2,3,-Dioxygenase / Q000378:metabolism; D007371:Interferon-gamma / Q000276:immunology* / Q000494:pharmacology; D019169:Jurkat Cells; D007963:Leukocytes, Mononuclear / Q000276:immunology / Q000382:microbiology*; D008214:Lymphocytes / Q000378:metabolism / Q000382:microbiology*; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D050296:Microbial Viability; D017471:Receptors, Interferon / Q000276:immunology; D013154:Spleen / Q000166:cytology; D000096743:Interferon gamma Receptor
chemical_list: D050503:Indoleamine-Pyrrole 2,3,-Dioxygenase; D007371:Interferon-gamma; D017471:Receptors, Interferon; D000096743:Interferon gamma Receptor