Blood-brain barrier invasion by group B Streptococcus depends upon proper cell-surface anchoring of lipoteichoic acid
J. Clin. Invest. Kelly S. Doran, et al. 115:2499 doi:10.1172/JCI23829 [Go to this article.]

Figure 5
Absence of TLR2 does not effect attenuation of the ΔiagA mutant. (A) Kaplan-Meier survival plot of WT C57BL/6 and TLR2^–/– mice infected with WT or ΔiagA mutant GBS. (B) Bacterial counts (CFU) in mouse blood (at 6 hours) and in brain and at time of death (48 hours). ^#Bacterial brain counts were not determined because all TLR2^–/– mice infected with WT GBS died before the experimental endpoint of 48 hours. (C) Detection of IL-8 released by hBMECs after stimulation with WT or ΔiagA mutant GBS using ELISA. (D) HMECs that expressed TLR2 or TLR4 were transfected with an NF-κB–luciferase reporter. Subsequently, cells were stimulated with 2 doses of GBS, and luciferase activity was determined by luminometry.