Chlamydophila pneumoniae attachment and infection in low proteoglycan expressing human lymphoid Jurkat cells
Chlamydophila pneumoniae attachment and infection in low proteoglycan expressing human lymphoid Jurkat cells
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DOI：
10.1016/j.micpath.2011.03.010
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发表时间：
2011-09-01
影响因子：
3.8
通讯作者：
Yamaguchi, Hiroyuki
中科院分区：
文献类型：
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作者：
Kobayashi, Miho;Ishida, Kasumi;Yamaguchi, Hiroyuki
本研究探讨了肺炎衣原体附着于淋巴细胞的蛋白聚糖依赖机制。淋巴Jurkat细胞和上皮HEp-2细胞静态感染肺炎支原体（TW183）。透射电镜和包涵形成单位的评估表明，细菌在Jurkat细胞中正常生长，能够产生继发性感染；然而，它们的生长速度比HEp-2细胞慢。RT-PCR分析表明，HEp-2细胞强烈表达pg核心蛋白编码基因，从而在细胞表面维持肝素等糖胺聚糖（GAGs）。除了glypican-1外，在Jurkat细胞中没有观察到类似的基因表达水平。免疫荧光分析也支持HEp-2细胞中肝素的高表达和Jurkat细胞中的低表达，尽管硫酸肝素预处理可以显著抑制细菌对这两种细胞的附着。用抗衣原体LPS和肝素抗体的免疫荧光共染色未发现Jurkat细胞上的细菌和肝素共定位。我们还证实，当肺炎衣原体静态感染人类CD4（+）外周血淋巴细胞时，已知未表达可检测到的肝素水平，细菌附着在细胞上并形成包涵体。因此，与HEp-2细胞相比，肺炎C与低PG表达的Jurkat细胞的附着机制是独特的，并且可能不依赖于肝素等gag。(C) 2011 Elsevier Ltd.版权所有。
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. (C) 2011 Elsevier Ltd. All rights reserved.