Penicillin G-Induced Chlamydial Stress Response in a Porcine Strain of Chlamydia pecorum

Figure 3

Penicillin G exposure prevents Chlamydia pecorum-mediated cell death and C. pecorum recovers infectivity upon discontinuation of penicillin exposure. C. pecorum-infected HeLa cells were penicillin G (PenG) exposed or diluent exposed (mock) from 0 to 35 hours postinfection (hpi). Cycloheximide was included (a) or not included (b, c) in the incubation medium. At 35 hpi, medium was changed to continue or discontinue (recovery, REC) penicillin exposure for 24 or 48 hours (h) and cycloheximide was maintained for (a). Inclusions were visualized and mean nuclei per field were determined as described for Figure 2. Representative immunofluorescence microscopic images illustrate cell death in mock-exposed controls, inclusions containing aberrant bodies upon continued penicillin exposure and normal-appearing inclusions upon recovery (REC). Production of infectious elementary bodies was determined by titration by subpassage and expressed as inclusion-forming units (IFU)/mL. Results are means ± standard deviation. The two-tailed t-test was used to compare means; p ≤ 0.05 = significant ; . Scale bars = 5 μm.

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