Figure 3.

C. trachomatisL2 response to heat shock includes increased levels of the HtrA protein and significant morphological alterations. (A) Transmission electron micrographs (TEM) of a C. trachomatis L2 infected HEp-2 cell (acute infection) at 23 h PI. (B) TEM of a C. trachomatis L2 infected HEp-2 cell which was shifted to 42°C for 3 h at 20 h PI (23 h PI). (C) Western blots for HtrA and MOMP against total cellular extracts from the acute and heat shock cultures. Samples are (HtrA polyclonal sera) 1: uninfected HEp-2 cells acute conditions, 2: C. trachomatis L2 infected HEp-2 cells acute (23 h PI), 3: uninfected HEp-2 cells heat shocked for 3 h at 42°C at 20 hours post infection, 4: C. trachomatis L2 infected HEp-2 cells heat shocked for 3 h at 42°C at 20 h PI; (MOMP monoclonal antibody) 5: uninfected HEp-2 cells acute conditions, 6: C. trachomatis L2 infected HEp-2 cells acute (23 h PI), 7: uninfected HEp-2 cells heat shocked for 3 h at 42°C at 20 h PI, 8: C. trachomatis L2 infected HEp-2 cells heat shocked for 3 h at 42°C at 20 h PI. The quantification of HtrA western blot band intensity was conducted using densiotometry, three separate experiments examined by western blot were used to quantify the difference in band intensities between acute and heat shock samples. The average of these three differences (heat shock:acute) is indicated to the right of the figure with the standard deviation indicated in parentheses.

Huston et al. BMC Microbiology 2008 8:190   doi:10.1186/1471-2180-8-190
Download authors' original image