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Chlamydia trachomatis serovar L2 infection model using human lymphoid Jurkat cells

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Title: Chlamydia trachomatis serovar L2 infection model using human lymphoid Jurkat cells
Authors: Kubo, Takeru Browse this author
Ishida, Kasumi Browse this author
Matsuo, Junji Browse this author →KAKEN DB
Nakamura, Shinji Browse this author →KAKEN DB
Hayashi, Yasuhiro Browse this author →KAKEN DB
Sakai, Haruna Browse this author
Yoshida, Mitsutaka Browse this author
Takahashi, Kaori Browse this author
Hirai, Itaru Browse this author
Yamamoto, Yoshimasa Browse this author
Yamaguchi, Hiroyuki Browse this author →KAKEN DB
Keywords: Chlamydia trachomatis
Serovar L2
Jurkat cells
Issue Date: Jul-2012
Publisher: Elsevier
Journal Title: Microbial Pathogenesis
Volume: 53
Issue: 1
Start Page: 1
End Page: 11
Publisher DOI: 10.1016/j.micpath.2012.02.005
PMID: 22516802
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.
Type: article (author version)
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)

Submitter: 山口 博之

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