Cobalt Alloy Implant Debris Induces Inflammation and Bone Loss Primarily through Danger Signaling, Not TLR4 Activation: Implications for DAMP-ening Implant Related Inflammation
Fig 5
Blocking TLR4 does not significantly decrease IL-1β and TNF-α response of human primary monocyte/macrophages to Cobalt-alloy particles.
(A) IL-1β and (B) TNF-α secreted by human primary monocytes/macrophages (n = 5) challenged with Cobalt-alloy particles (particles:cell = 5:1), LPS or Alum (NLRP3 inflammasome activator) for 20 h, with or without ZVAD-FMK (caspase-1 inhibitor) or PAb TLR4 antibody and was quantified by ELISA. Cytokine levels with use of PAb TLR4 are represented as percent increase as compared to respective control cells and averaged as a group. Note: * p<0.05 to each treatment groups respective control values.