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. 2007 Sep 6;4(4):223–231. doi: 10.7150/ijms.4.223

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© Ivyspring International Publisher. This is an open-access article distributed under the terms of the Creative Commons License (http://creativecommons.org/licenses/by-nc-nd/3.0/). Reproduction is permitted for personal, noncommercial use, provided that the article is in whole, unmodified, and properly cited.

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Fig 1 — Induction of productive infection by Chlamydia trachomatis in trophoblast. The formation of Chlamydia trachomatis inclusion (MOI = 3/cell) in trophoblast (A) compared with direct infection of HEp-2 cells (B) is represented. Experimental procedure was repeated three times. Panel (A) indicates HEp-2 cell infection with Chlamydia trachomatis that has been harvested from trophoblast cell line JAR and titrated onto HEp-2 cells. Panel (B) shows a direct infection of HEp-2 cells with Chlamydia trachomatis. Notice the relative suppression of Chlamydia trachomatis growth in trophoblast. The arrows indicate Chlamydia trachomatis inclusion bodies. However, the Chlamydia trachomatis harvested from trophoblast were able to efficiently infect HEp-2 cells (productive infection), (C) although there is a significant difference (p < 0.01 *) in IFU/ml when Chlamydia trachomatis harvested from trophoblast are compared with regular EBs in our laboratory are used to infect HEp-2 cells (C). Further, percent infectivity of HEp-2 cells is shown in (D). There is a significant difference (p < 0.01 *) between direct infection of HEp-2 cells (red) and infection of HEp-2 cells with Chlamydia trachomatis harvested from trophoblast. All values represent means ± SEM (n = 3).

Fig 1 — Induction of productive infection by Chlamydia trachomatis in trophoblast. The formation of Chlamydia trachomatis inclusion (MOI = 3/cell) in trophoblast (A) compared with direct infection of HEp-2 cells (B) is represented. Experimental procedure was repeated three times. Panel (A) indicates HEp-2 cell infection with Chlamydia trachomatis that has been harvested from trophoblast cell line JAR and titrated onto HEp-2 cells. Panel (B) shows a direct infection of HEp-2 cells with Chlamydia trachomatis. Notice the relative suppression of Chlamydia trachomatis growth in trophoblast. The arrows indicate Chlamydia trachomatis inclusion bodies. However, the Chlamydia trachomatis harvested from trophoblast were able to efficiently infect HEp-2 cells (productive infection), (C) although there is a significant difference (p < 0.01 *) in IFU/ml when Chlamydia trachomatis harvested from trophoblast are compared with regular EBs in our laboratory are used to infect HEp-2 cells (C). Further, percent infectivity of HEp-2 cells is shown in (D). There is a significant difference (p < 0.01 *) between direct infection of HEp-2 cells (red) and infection of HEp-2 cells with Chlamydia trachomatis harvested from trophoblast. All values represent means ± SEM (n = 3).