Skin Interface, a Key Player for Borrelia Multiplication and Persistence in Lyme Borreliosis

Bernard, Quentin; Grillon, Antoine; Lenormand, C.; Ehret‐Sabatier, Laurence; Boulanger, Nathalie

doi:10.1016/j.pt.2019.12.017

Cited by 24 publications

(28 citation statements)

References 93 publications

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“…Tick saliva may be injected in the epidermis, dermis, or the epidermis/dermis border depending on the tick mouthpart apparatus 4 , 49 . The γδ T cell population in the mouse skin is constituted of two distinct subpopulations, including dermal γδ T cells (also known as γδ T17 cells) that express the T cell receptor Vγ4 or Vγ6 30 , 50 , and DETCs that express the T cell receptor Vγ5Vδ1 in the epidermis 28 , according to the Heilig and Tonegawa nomenclature 51 .…”

Section: Resultsmentioning

confidence: 99%

Tick extracellular vesicles enable arthropod feeding and promote distinct outcomes of bacterial infection

et al. 2021

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Extracellular vesicles are thought to facilitate pathogen transmission from arthropods to humans and other animals. Here, we reveal that pathogen spreading from arthropods to the mammalian host is multifaceted. Extracellular vesicles from Ixodes scapularis enable tick feeding and promote infection of the mildly virulent rickettsial agent Anaplasma phagocytophilum through the SNARE proteins Vamp33 and Synaptobrevin 2 and dendritic epidermal T cells. However, extracellular vesicles from the tick Dermacentor andersoni mitigate microbial spreading caused by the lethal pathogen Francisella tularensis. Collectively, we establish that tick extracellular vesicles foster distinct outcomes of bacterial infection and assist in vector feeding by acting on skin immunity. Thus, the biology of arthropods should be taken into consideration when developing strategies to control vector-borne diseases.

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Section: Resultsmentioning

confidence: 99%

Tick extracellular vesicles enable arthropod feeding and promote distinct outcomes of bacterial infection

et al. 2021

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“…As the presence of complement in vertebrate blood, our findings raise a possibility that spirochetes must evade host complement specifically in the blood meal. However, tick feeding on live animals may introduce confounding factors of blood meal-independent, complement-mediated clearance (59). Using different sources of blood in “artificial feeding chambers” without the involvement of animals allows us to demonstrate that spirochete evasion to complement in blood meals dictates Lyme borreliae host tropism (29).…”

Section: Discussionmentioning

confidence: 99%

Host tropism determination by convergent evolution of immunological evasion in the Lyme disease system

Hart

Dupuis

Tufts

et al. 2021

Preprint

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Microparasites selectively adapt in some hosts, known as host tropism. Transmitted through ticks and carried mainly by mammals and birds, the Lyme disease (LD) bacterium is a well-suited model to study such tropism. LD bacteria species vary in host ranges through mechanisms eluding characterization. By feeding ticks infected with different LD bacteria species, utilizing feeding chambers and live mice and quail, we found species-level differences of bacterial transmission. These differences localize on the tick blood meal, and complement, a defense in vertebrate blood, and a bacterial polymorphic protein, CspA, which inactivates complement by binding to a host complement inhibitor, FH. CspA selectively confers bacterial transmission to vertebrates that produce FH capable of allele-specific recognition. Phylogenetic analyses revealed convergent evolution as the driver of such findings, which likely emerged during the last glacial maximum. Our results identify LD bacterial determinants of host tropism, defining an evolutionary mechanism that shapes host-microparasite associations.

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“…The manifestations of B. burgdorferi infection vary significantly between animal species and by tissue types. The skin is composed of multiple cell types able to detect B. burgdorferi, including resident cells such as fibroblasts (26). Skin fibroblasts have been shown to express many proinflammatory cytokines and chemokines in response to B. burgdorferi in vitro (27).…”

Section: Discussionmentioning

confidence: 99%

Innate Immune Memory to Repeated Borrelia burgdorferi Exposure Correlates with Murine In Vivo Inflammatory Phenotypes

Bernard

2020

The Journal of Immunology

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Borrelia burgdorferi, the causative agent of Lyme disease, is transmitted by the bite of an infected tick. Once inoculated into the host dermis, it disseminates to various organs including distant skin sites, the heart, the joint and the nervous system. Most humans will develop an early skin manifestation called erythema migrans at the tick bite site. This can be followed by symptoms such as carditis, neuritis, meningitis, or arthritis if not treated. A specific mouse strain, C3H/HeN develops arthritis with B. burgdorferi infection whereas another strain, C57BL/6, develops minimal to no arthritis. Neither strain of mice show any skin signs of rash or inflammation. Factors that determine the presence of skin inflammation and the joint arthritis susceptibility in the host are only partially characterized. We show in this study that murine fibroblast-like synoviocytes display trained immunity, a program in some cells that results in increased inflammatory responses if the cell has previously come in contact with a stimulus, and that trained immunity in fibroblast-like synoviocytes tested ex vivo correlates with Lyme arthritis susceptibility. Conversely, skin fibroblasts do not exhibit trained immunity, which correlates with the absence of skin symptoms in these mice. Moreover, we demonstrate that the trained phenotype in FLS is affected by the cell environment, which depends on the host genetic background. Future studies expanding this initial report of the role of trained immunity on symptoms of B. burgdorferi infection may provide insight into the pathogenesis of disease in murine models.

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Skin Interface, a Key Player for Borrelia Multiplication and Persistence in Lyme Borreliosis

Cited by 24 publications

References 93 publications

Tick extracellular vesicles enable arthropod feeding and promote distinct outcomes of bacterial infection

Tick extracellular vesicles enable arthropod feeding and promote distinct outcomes of bacterial infection

Host tropism determination by convergent evolution of immunological evasion in the Lyme disease system

Innate Immune Memory to Repeated Borrelia burgdorferi Exposure Correlates with Murine In Vivo Inflammatory Phenotypes

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