摘要：SummaryBorrelia burgdorferi(Bb), a vector-borne bacterial pathogen and the causative agent of Lyme disease, can spread to distant tissues in the human host by traveling in and through monolayers of endothelial cells (ECs) lining the vasculature. To examine whetherBbalters the physical forces of ECs to promote its dissemination, we exposed ECs toBband observed a sharp and transient increase in EC traction and intercellular forces, followed by a prolonged decrease in EC motility and physical forces. All variables returned to baseline at 24 h after exposure. RNA sequencing analysis revealed an upregulation of innate immune signaling pathways during early but not lateBbexposure. Exposure of ECs to heat-inactivatedBbrecapitulated only the early weakening of EC mechanotransduction. The differential responses to live versus heat-inactivatedBbindicate a tight interplay between innate immune signaling and physical forces in host ECs and suggest their active modulation byBb.Graphical abstractDisplay OmittedHighlights•Early exposure toBorreliadecreases endothelial cell motility and physical forces•Early exposure toBorreliaalso upregulates the host’s innate immune signaling pathways•Host cell mechanics and signaling return to steady state at late exposure times•Exposure to dead bacteria steadily reduces motility and physical forces of host cellsImmunology; Microbiology; Cell biology; Biophysics; Transcriptomics
