ArticleInfection and immunity2003
The urokinase receptor can be induced by Borrelia burgdorferi through receptors of the innate immune system.
Article in Infection and immunity, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed.
- Plasminogen activator receptor assemblies in cell signaling, innate immunity, and inflammation.American journal of physiology. Cell physiology · 2021Review
- Endogenous and Borrowed Proteolytic Activity in theMicrobiology and molecular biology reviews : MMBR · 2021Review
- Article
- A multi-omic analysis reveals the regulatory role of CD180 during the response of macrophages to Borrelia burgdorferi.Emerging microbes & infections · 2018Article
- Toll-like receptor cascade and gene polymorphism in host-pathogen interaction in Lyme disease.Journal of inflammation research · 2016Review
- The HtrA protease of Borrelia burgdorferi degrades outer membrane protein BmpD and chemotaxis phosphatase CheX.Molecular microbiology · 2013Article
- The enolase of Borrelia burgdorferi is a plasminogen receptor released in outer membrane vesicles.Infection and immunity · 2012Article
- Utility of the plasma level of suPAR in monitoring risk of mortality during TB treatment.PloS one · 2012Article
- Interleukin-10 alters effector functions of multiple genes induced by Borrelia burgdorferi in macrophages to regulate Lyme disease inflammation.Infection and immunity · 2011Article
- OspA-CD40 dyad: ligand-receptor interaction in the translocation of neuroinvasive Borrelia across the blood-brain barrier.Scientific reports · 2011Article
- The receptor for urokinase regulates TLR2 mediated inflammatory responses in neutrophils.PloS one · 2011Article
- Novel Diagnosis of Lyme Disease: Potential for CAM Intervention.Evidence-based complementary and alternative medicine : eCAM · 2009Article
- Article
- The urokinase receptor (uPAR) facilitates clearance of Borrelia burgdorferi.PLoS pathogens · 2009Article
- Post-transcriptional regulation of urokinase-type plasminogen activator receptor expression in lipopolysaccharide-induced acute lung injury.American journal of respiratory and critical care medicine · 2009Article
- Phagocytosis of Borrelia burgdorferi, the Lyme disease spirochete, potentiates innate immune activation and induces apoptosis in human monocytes.Infection and immunity · 2008Article
- The Pseudomonas aeruginosa LasB metalloproteinase regulates the human urokinase-type plasminogen activator receptor through domain-specific endoproteolysis.Infection and immunity · 2007Article
- Borrelia burgdorferi, host-derived proteases, and the blood-brain barrier.Infection and immunity · 2005Article
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
Monocytic cells exposed to Borrelia burgdorferi, through unknown receptors, overexpress the urokinase receptor (uPAR), a key mediator of the plasminogen activation system. We show that combined blockade of CD14 and TLR2 causes a significant inhibition of B. burgdorferi-induced uPAR in Mono Mac 6 (MM6) cells. Other pattern recognition receptors tested (CD11b/CD18, the mannose receptor, and the N-formyl-methionyl-leucyl-phenylalanine receptor) did not have demonstrated roles in B. burgdorferi-mediated uPAR induction. We dissected the result for CD14 andTLR2 by investigating the singular contributions of each. Independent functional blockade of CD14 or TLR2 failed to inhibit B. burgdorferi-mediated uPAR induction. 1,25-Dihydroxyvitamin D(3) differentiation of MM6 cells increased CD14 expression 12-fold but did not augment B. burgdorferi-mediated uPAR expression. Peritoneal exudate macrophages (PEM) from CD14- or TLR2-deficient mice were not defective in B. burgdorferi-mediated synthesis of uPAR mRNA and protein. Increased uPAR mRNA or protein or both were apparent in PEM from transgenic and control mice, even at a ratio of one Borrelia spirochete per cell. We conclude that signaling for the uPAR response, as mediated by B. burgdorferi, proceeds with CD14 and TLR2 as partial contributors. That part under control of CD14 and TLR2 represents a new link between the host plasminogen activation and innate immunity systems.
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