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 |
lymphocytes |
Jurkat cells |
heparin |
proteoglycans |
glycosaminoglycans |
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) |
URI: | http://hdl.handle.net/2115/47049 |
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)
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