title: Ixodes tick saliva suppresses the keratinocyte cytokine response to TLR2/TLR3 ligands during early exposure to Lyme borreliosis.
abstract: Ixodes hard tick induces skin injury by its sophisticated biting process. Its saliva plays a key role to enable an efficient blood meal that lasts for several days. We hypothesized that this feeding process may also be exploited by pathogens to facilitate their transmission, especially in the context of arthropod-borne diseases. To test this, we used Lyme borreliosis as a model. This bacterial infection is caused by Borrelia burgdorferi sensu lato transmitted by Ixodes. We co-incubated Borrelia with human keratinocytes in the presence of poly (I: C), a dsRNA TLR3 agonist generated by skin injury. This induced a strong cytokine response from human primary keratinocytes that was much greater than that induced by Borrelia alone. OspC, a TLR2/1 agonist and a major surface lipoprotein of Borrelia also amplified the process. Interestingly, tick saliva inhibited cytokine responses by keratinocytes to these TLR agonists. We propose that Borrelia uses the immunoprivileged site produced by tick saliva to facilitate its transmission.
authors: EA7290 Virulence bactérienne précoce: groupe borréliose de Lyme, Fédération de médecine Translationnelle et Faculté de Pharmacie de Strasbourg, Université de Strasbourg, Strasbourg, France.
authors: Quentin
authors: Q
authors: Bernard
authors: Department of Dermatology, University of California, San Diego, CA, USA.
authors: Richard L
authors: RL
authors: Gallo
authors: EA7290 Virulence bactérienne précoce: groupe borréliose de Lyme, Fédération de médecine Translationnelle et Faculté de Pharmacie de Strasbourg, Université de Strasbourg, Strasbourg, France.|Centre National de Reference Borrelia, Centre Hospitalier Universitaire, Strasbourg, France.
authors: Benoît
authors: B
authors: Jaulhac
authors: Department of Dermatology, University of California, San Diego, CA, USA.
authors: Teruaki
authors: T
authors: Nakatsuji
authors: Department of Medicine, State University of New York, Stony Brook, NY, USA.
authors: Benjamin
authors: B
authors: Luft
authors: Department of Medicine, State University of New York, Stony Brook, NY, USA.
authors: Xiahoua
authors: X
authors: Yang
authors: EA7290 Virulence bactérienne précoce: groupe borréliose de Lyme, Fédération de médecine Translationnelle et Faculté de Pharmacie de Strasbourg, Université de Strasbourg, Strasbourg, France.|Centre National de Reference Borrelia, Centre Hospitalier Universitaire, Strasbourg, France.
authors: Nathalie
authors: N
authors: Boulanger
mesh_terms: D000818:Animals; D000942:Antigens, Bacterial / Q000378:metabolism; D017209:Apoptosis; D001425:Bacterial Outer Membrane Proteins / Q000378:metabolism; D025065:Borrelia burgdorferi; D049109:Cell Proliferation; D002478:Cells, Cultured; D016207:Cytokines / Q000378:metabolism; D006801:Humans; D007249:Inflammation; D018884:Ixodes; D015603:Keratinocytes / Q000166:cytology / Q000378:metabolism / Q000382:microbiology; D008024:Ligands; D008193:Lyme Disease / Q000276:immunology; D051379:Mice; D008810:Mice, Inbred C57BL; D011070:Poly I-C / Q000737:chemistry; D012330:RNA, Double-Stranded / Q000737:chemistry; D012463:Saliva / Q000382:microbiology*; D012867:Skin / Q000276:immunology / Q000293:injuries / Q000382:microbiology; D012871:Skin Diseases / Q000276:immunology / Q000382:microbiology*; D051195:Toll-Like Receptor 2 / Q000378:metabolism*; D051196:Toll-Like Receptor 3 / Q000378:metabolism*
chemical_list: D000942:Antigens, Bacterial; D001425:Bacterial Outer Membrane Proteins; D016207:Cytokines; D008024:Ligands; C079616:OspC protein; D012330:RNA, Double-Stranded; D051195:Toll-Like Receptor 2; D051196:Toll-Like Receptor 3; D011070:Poly I-C
keywords: TLR2; TLR3; borrelia; lyme; ticks