This study reports the direct observation of catch bonds involving cell-adhesion molecules. Using atomic force microscopy and flow-chamber experiments, the researchers showed that increasing force first prolonged and then shortened the lifetimes of P-selectin complexes with P-selectin glycoprotein ligand-1 (PSGL-1), revealing both catch and slip bond behavior. This dual response to force provides a mechanism for regulating cell adhesion under conditions of variable mechanical stress. The results suggest that the P-selectin-PSGL-1 interaction behaves as catch bonds in the low force range and as slip bonds in the high force range. The findings demonstrate that the P-selectin-PSGL-1 interaction is specific for catch-slip transitional bonds, which may explain why leukocyte rolling on selectins first increases and then decreases as wall shear stress increases. The study also shows that the P-selectin-PSGL-1 interaction is specific for catch-slip transitional bonds, which may explain why platelet tethering to von Willebrand factor on disrupted vessels is most effective at higher shear stresses at the arterial wall. The results suggest that catch bonds may be important for regulating cell adhesion during mechanical stress. The study was supported by grants from the Office of Naval Research, the Defense Advanced Research Project Agency and the National Institutes of Health.This study reports the direct observation of catch bonds involving cell-adhesion molecules. Using atomic force microscopy and flow-chamber experiments, the researchers showed that increasing force first prolonged and then shortened the lifetimes of P-selectin complexes with P-selectin glycoprotein ligand-1 (PSGL-1), revealing both catch and slip bond behavior. This dual response to force provides a mechanism for regulating cell adhesion under conditions of variable mechanical stress. The results suggest that the P-selectin-PSGL-1 interaction behaves as catch bonds in the low force range and as slip bonds in the high force range. The findings demonstrate that the P-selectin-PSGL-1 interaction is specific for catch-slip transitional bonds, which may explain why leukocyte rolling on selectins first increases and then decreases as wall shear stress increases. The study also shows that the P-selectin-PSGL-1 interaction is specific for catch-slip transitional bonds, which may explain why platelet tethering to von Willebrand factor on disrupted vessels is most effective at higher shear stresses at the arterial wall. The results suggest that catch bonds may be important for regulating cell adhesion during mechanical stress. The study was supported by grants from the Office of Naval Research, the Defense Advanced Research Project Agency and the National Institutes of Health.