Figure 6.

rTsCRT-S inhibited C1q-triggered neutrophil chemotaxis and function. (A) C1q-induced neutrophil chemotaxis was inhibited by rTsCRT-S in a transwell migration chamber. The number of cells traversing the membrane was counted. (B) rTsCRT-S inhibited dHL60 cell release of ROS and (C) neutrophil elastase (NE) through binding to C1q. DCFH-DA was used to probe ROS production, and NE substrate was used to evaluate NE production, which was also quantified as MFI. SPCK was used as an NE inhibitor and cysteamine used as a ROS inhibitor. (D) C1q-mediated neutrophil killing of NBL was inhibited by rTsCRT-S. ATP activity was measured as a marker for NBL viability. ATP levels were calculated using a standard curve generated from the ATP levels in untreated control NBL. Each experiment was repeated three times. Data are shown as the mean ± SEM (*p < 0.05, **p < 0.01, ***p < 0.001, and ****p < 0.0001; ns = no significant difference).