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. 2009 Apr 15;4(4):e5191. doi: 10.1371/journal.pone.0005191

Figure 12. Low (28°C) temperature induced persistent infection of culture cells with C. trachomatis does not block PmpD post-translational processing.

Figure 12

McCoy cells were infected with C. trachomatis serovar L2, fixed with methanol at 24 (A and D) h p.i. at 37°C and 48 (B and E) and 120 (C and F) h p.i. at 28°C and reacted with mAb against chlamydial MOMP (green) in combination with pAb against fragment 2 of PmpD (red) (A–C) or pAb against chlamydial HSP60 protein (red) (D–F) (internal control). RBs produced during persistent infection are abnormally large with thin cell wall (B–C and E–F) compared with uniformly sized and round shaped RBs (A and D) produced during normal infection. Arrow indicates localization of PmpD during the chlamydial life cycle on the surface of aberrant RBs (A) or in the inclusion lumen outside Chlamydia (red spots) (B). When reacted with anti-HSP60 pAb, no material was visible outside Chlamydia. Note that the rate of PmpD secretion outside Chlamydia is much lower and slower when compared with normal (37°C) infection. The photographs were made using a Leica SL confocal microscope.