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Fig. 6 | Journal of Neuroinflammation

Fig. 6

From: PKR deficiency alters E. coli-induced sickness behaviors but does not exacerbate neuroimmune responses or bacterial load

Fig. 6

Loss of PKR did not enhance bacterial load. Lavage fluid (injection site) and blood were sampled at the indicated time points. In (a), serially diluted lavage samples from E. coli-challenged mice were plated onto bacterial agar plates and incubated at 37 °C for 24 h. The numbers of colony-forming units (CFU) were similar between WT and PKR−/− mice throughout the time points; n = 17–19 per group. There was no CFU detected in the lavage fluid from the PBS-injected mice. In (b), purified lavage fluid from E. coli-infected animals were tested for their bacterial 16S rDNA levels, and expressed as fold of baseline (i.e., PBS-injected animals). Similar levels of 16S rDNA were observed between WT and PKR−/− animals; n = 13–18 per group. In (c), anti-coagulated blood was collected from mice at 48 h, purified, and assessed for 16S rDNA. No significant increase of 16S rDNA could be found in the purified blood samples of the two infected groups as compared to the WT PBS group; n = 3 per group. We also could not culture any bacterial colonies from blood sampled at this time point

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