作者: Joppe WR Hovius , Maarten F Bijlsma , Gerritje JW van der Windt , W Joost Wiersinga , Bastiaan JD Boukens
DOI: 10.1371/JOURNAL.PPAT.1000447
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摘要: The causative agent of Lyme borreliosis, the spirochete Borrelia burgdorferi, has been shown to induce expression urokinase receptor (uPAR); however, role uPAR in immune response against never investigated. not only acts as a proteinase receptor, but can also, dependently or independently ligation uPA, directly affect leukocyte function. We here demonstrate that is upregulated on murine and human leukocytes upon exposure B. burgdorferi both vitro well vivo. Notably, burgdorferi-inoculated C57BL/6 knock-out mice harbored significantly higher numbers compared WT controls. This was associated with impaired phagocytotic capacity by vitro. vivo, vitro, were unaltered tPA (low fibrinolytic activity) PAI-1 (high Strikingly, partially backcrossed susceptible C3H/HeN background, more severe carditis increased local TLR2 IL-1β mRNA expression. In conclusion, infection, required for phagocytosis adequate eradication from heart mechanism independent binding uPA its system.