Figure 5. EGR1 signaling has a significant impact on S. aureus skin infection.

a, Back skin abscess model. Mice were shaved on the back and infected with 1 × 10⁷ CFU of the indicated bacteria in 50 μl of PBS subcutaneously into the left and right flank. Abscess sizes were measured daily. n=8–10/group. Statistical analysis is by repeated measures 2-way ANOVA (or mixed model) with Tukey’s post-tests. Results of the statistical analysis are shown using asterisks (****, p<0.0001; ***, p<0.001; **, p<0.01; *, p<0.05) with the colors indicating the group against which the post-tests compared the LAC-infected EGR1^−/− group. No comparisons other than those indicated versus the LAC-infected EGR1^−/− mice group were statistically significant. Error bars show the mean ± SD. b, Representative examples of abscesses on day 3. Abscesses were selected that were close to the average size within each group. c, Model comparing the canonical (right) versus the EGR1-mediated, toxin-triggered mechanism of leukocyte attraction to the infection site (left). The EGR1-mediated mechanism directly senses secreted, pathogen-derived molecules (PSMs) as opposed to the surface-located molecules (lipopolysaccharide, lipoteichoic acid, and others) that are widely conserved throughout Gram-positive or Gram-negative bacteria and sensed commonly by receptors of the Toll-like receptor (TLR) family in the canonical pathway. In contrast to the canonical pathway, which cannot distinguish between bacteria with different pathogenicity, the EGR1-mediated pathway is thus pathogen-specific and not dependent on the prior activation of and cytokine release by resident skin cells.