Tnfrsf21 which was identified by [ 33] as potential candidate of Qivr17-2 also exhibits a cis-eQTL in non-infected BXD mice [ 26] but was not found to be regulated in C57BL/6 mice after infection (data not published).
In line with the bacterial loads, no differences were seen in total cell count or neutrophil influx in BALF between DNase-treated and untreated mice after infection (data not shown).
D.R. and S.C. performed SNP analyses and database management, with the support of G.S. C.R., A.P., W.F., R.S., A.-S.D., E.W., A. Cascioferro and M.-C.G. performed mouse infection experiments, in vivo data analyses and/or mycobacterial growth assays.
As expected, the control strain with the transposon Tn5EZ insertion in purA was unable to grow in the absence of exogenous purines (Fig. S2) and was also avirulent in the mouse sepsis model of infection (data not shown).
To test potential IFNγ regulation of PD-L expression on DCs during BCG infection, we infected IFNγ KO mice, but observed no differences in PD-L expression compared to wild-type mice six weeks after infection (data not shown).
Likewise, there were no differences in serum ALT levels between B6 and IL-22 KO mice during secondary LM infection (data not shown), suggesting that IL-22 is not required for limiting liver damage.
In contrast to the wild type strain, which reached high bacterial loads in all organs within 48 hours, Kim53ΔnlpD could not be detected in the draining inguinal lymph nodes (I-LN), the spleen, the lungs or the blood of the subcutaneously infected mice at 24 hours post infection (data not shown) and up to 10 days post infection (Fig. 6A).
Our final analysis therefore includes 104 observations of the system (including biological replicates for macaque and mouse); the Calu-3 cell infection data (two sets of 6 time points), data from each viral strain in macaque (four time points, four viruses, two replicates), and each dosage in mouse (four time points, three dosages, five replicates).
The conflicting data from mouse infection models and the relative insensitivity of murine polymorphonuclear leukocytes (PMNs or granulocytes) to the leukolytic effect of PVL compared with human cells prompted us to assess the role of PVL in CA-MRSA pathogenesis in a rabbit model.
