Skip to main content
. 2011 Sep;3(9):545–558. doi: 10.1002/emmm.201100158

Figure 2. IsoQC is the major pE1-CCL2 forming enzyme in vivo.

Figure 2

  1. Analysis of the ratio of total-CCL2 and pE1-CCL2 secreted from LPS-stimulated primary cells isolated from QC−/− mice compared to WT littermates (QC+/+; n = 4–5, mean ± SEM).
  2. Analysis of the ratio of total-CCL2 and pE1-CCL2 secreted from LPS-stimulated primary cells isolated from isoQC−/− mice compared to WT littermates (isoQC+/+; ***p < 0.001 vs. isoQC+/+, Student's t-test, n = 4, mean ± SEM).
  3. pE1-CCL2 formation in serum after peripheral injection of LPS in male QC−/− mice compared to WT littermates (QC+/+; n = 6–7, mean ± SEM).
  4. pE1-CCL2 formation in serum after peripheral injection of LPS in male isoQC−/− mice, compared to WT littermates (QC+/+; ***p < 0.001 vs. isoQC+/+ +LPS, Student's t-test, n = 5–8, mean ± SEM).
  5. IsoQC-deficiency leads to impaired monocyte recruitment to lungs after intranasal LPS-application in isoQC−/− compared to WT littermates (isoQC+/+; *p < 0.05 vs. isoQC+/+ +LPS, Student's t-test, n = 7–8, mean ± SEM).
  6. Analysis of neutrophils in bronchoalveolar fluid after intranasal LPS-application in isoQC−/− compared to WT littermates (isoQC+/+; n = 7–8, mean ± SEM).