title: Chlamydia trachomatis serovar L2 infection model using human lymphoid Jurkat cells.
abstract: Chlamydia trachomatis L2 invasively attacks lymphatic and subepithelial tissues of the genital tract during the formation of primary lesions. This subsequently results in lymphadenopathy, and suggests a greater propensity for systemic dissemination. However, whether lymphocytes are a potential vehicle cell for the dissemination of this infection remains unknown. We therefore assessed the growth properties of C. trachomatis L2 in lymphoid Jurkat cells compared with those observed in epithelial HeLa cells. Both cells supported the growth of C. trachomatis with a similar increase in infective progenies. Enriched human-blood lymphocytes also supported the C. trachomatis growth as well as Jurkat cells. Bacteria infecting the Jurkat cells were more susceptible to antibiotics (doxycycline, azithromycin, ofloxacin) than those in HeLa cells. Of the sphingomyelin biosynthesis inhibitors tested, both myriocin and fumonisin B1 significantly inhibited bacterial growth in both cells types. A Jurkat cell mutant that impaired bacterial growth was established using ethylmethanesulfonate treatment. DNA microarray analysis with real-time reverse transcription-polymerase chain reaction revealed that the mutant cells over-expressed granzyme K gene. Immunofluorescence staining also indicated that granzyme K irregularly over-expressed among the mutant cells as compared with that of the wild cells, suggesting a possible mechanism refractory to C. trachomatis infection. Thus, we concluded that C. trachomatis L2 could infect Jurkat cells with lymphoid properties, providing a new tool for studying C. trachomatis dissemination to tissues via lymphocyte movement.
authors.affiliation: Department of Medical Laboratory Sciences, Faculty of Health Sciences, Hokkaido University, Nishi-5 Kita-12 Jo, Kita-ku, Sapporo, Hokkaido 060-0812, Japan.
authors.forename: Takeru
authors.initials: T
authors.lastname: Kubo
authors.forename: Kasumi
authors.initials: K
authors.lastname: Ishida
authors.forename: Junji
authors.initials: J
authors.lastname: Matsuo
authors.forename: Shinji
authors.initials: S
authors.lastname: Nakamura
authors.forename: Yasuhiro
authors.initials: Y
authors.lastname: Hayashi
authors.forename: Haruna
authors.initials: H
authors.lastname: Sakai
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: Hiroyuki
authors.initials: H
authors.lastname: Yamaguchi
mesh_terms: D000900:Anti-Bacterial Agents / Q000494:pharmacology; D002692:Chlamydia trachomatis / Q000187:drug effects / Q000254:growth & development / Q000472:pathogenicity*; D005229:Fatty Acids, Monounsaturated / Q000494:pharmacology; D037341:Fumonisins / Q000494:pharmacology; D020869:Gene Expression Profiling; D006367:HeLa Cells; D006801:Humans; D019169:Jurkat Cells; D046228:Microarray Analysis; D008954:Models, Biological; D060888:Real-Time Polymerase Chain Reaction; D013601:T-Lymphocytes / Q000382:microbiology*
chemical_list: D000900:Anti-Bacterial Agents; D005229:Fatty Acids, Monounsaturated; D037341:Fumonisins; C056933:fumonisin B1; C001996:thermozymocidin