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Chlamydophila pneumoniae attachment and infection in low proteoglycan expressing human lymphoid Jurkat cells

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Title: Chlamydophila pneumoniae attachment and infection in low proteoglycan expressing human lymphoid Jurkat cells
Authors: Kobayashi, Miho Browse this author
Ishida, Kasumi Browse this author
Matsuo, Junji Browse this author →KAKEN DB
Nakamura, Shinji Browse this author →KAKEN DB
Nagasawa, Ayumi Browse this author
Motohashi, Kazuki Browse this author
Yao, Takashi Browse this author
Hirai, Itaru Browse this author
Yamamoto, Yoshimasa Browse this author
Suzuki, Haruki Browse this author
Shimizu, Chikara Browse this author →KAKEN DB
Matsuno, Kazuhiko Browse this author →KAKEN DB
Yamaguchi, Hiroyuki Browse this author →KAKEN DB
Keywords: Chlamydophila pneumoniae
Jurkat cells
Issue Date: Sep-2011
Publisher: Elsevier
Journal Title: Microbial Pathogenesis
Volume: 51
Issue: 3
Start Page: 209
End Page: 216
Publisher DOI: 10.1016/j.micpath.2011.03.010
PMID: 21511028
Abstract: This study investigated the proteoglycan (PG)-dependent mechanism of Chlamydophila pneumoniae attachment to lymphocytic cells. Lymphoid Jurkat cells and epithelial HEp-2 cells were statically infected with C. pneumoniae (TW183). Transmission electron microscopy and assessment of inclusion-forming units indicated that the bacteria grew normally in Jurkat cells and were capable of producing secondary infection; however, they grew at a slower rate than in HEp-2 cells. RT-PCR analysis indicated that HEp-2 cells strongly expressed PG-core protein encoding genes, thereby sustaining glycosaminoglycans (GAGs), such as heparin, on the cellular surface. Similar gene expression levels were not observed in Jurkat cells, with the exception of glypican-1. Immunofluorescence analysis also supported strong heparin expression in HEp-2 cells and minimal expression in Jurkat cells, although heparan sulfate pretreatment significantly inhibited bacterial attachment to both cell types. Immunofluorescent co-staining with antibodies against chlamydial LPS and heparin did not identify bacterial and heparin co-localization on Jurkat cells. We also confirmed that when C. pneumoniae was statically infected to human CD4(+) peripheral blood lymphocytes known not expressing detectable level of heparin, the bacteria attached to and formed inclusion bodies in the cells. Thus, the attachment mechanism of C. pneumoniae to Jurkat cells with low PG expression is unique when compared with HEp-2 cells and potentially independent of GAGs such as heparin.
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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