Lyme Disease Pathogenesis.
Jenifer Coburn,Brandon L. Garcia,Linden T. Hu,Mollie W. Jewett,Peter Kraiczy,Steven J. Norris,Jon T. Skare +6 more
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TLDR
An overview of virulence mechanisms and determinants for which roles have been demonstrated in vivo, primarily in mouse models of infection is provided.Abstract:
Lyme disease Borrelia are obligately parasitic, tick- transmitted, invasive, persistent bacterial pathogens that cause disease in humans and non-reservoir vertebrates primarily through the induction of inflammation. During transmission from the infected tick, the bacteria undergo significant changes in gene expression, resulting in adaptation to the mammalian environment. The organisms multiply and spread locally and induce inflammatory responses that, in humans, result in clinical signs and symptoms. Borrelia virulence involves a multiplicity of mechanisms for dissemination and colonization of multiple tissues and evasion of host immune responses. Most of the tissue damage, which is seen in non-reservoir hosts, appears to result from host inflammatory reactions, despite the low numbers of bacteria in affected sites. This host response to the Lyme disease Borrelia can cause neurologic, cardiovascular, arthritic, and dermatologic manifestations during the disseminated and persistent stages of infection. The mechanisms by which a paucity of organisms (in comparison to many other infectious diseases) can cause varied and in some cases profound inflammation and symptoms remains mysterious but are the subjects of diverse ongoing investigations. In this review, we provide an overview of virulence mechanisms and determinants for which roles have been demonstrated in vivo, primarily in mouse models of infection.read more
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Infection and immunity
TL;DR: Mutation of the Maturase Lipop Protein Attenuates the Virulence of Streptococcus equi to a Greater Extent than Does Loss of General Lipoprotein Lipidation.
HtrA, a Temperature- and Stationary Phase-Activated Protease Involved in Maturation of a Key Microbial Virulence Determinant, Facilitates Borrelia burgdorferi Infection in Mammalian Hosts
Meiping Ye,Meiping Ye,Kavita Sharma,Meghna Thakur,Alexis A. Smith,Özlem Büyüktanir,Xuwu Xiang,Xiuli Yang,Kamoltip Promnares,Yongliang Lou,X. Frank Yang,Utpal Pal +11 more
TL;DR: It is shown that transcript abundance as well as proteolytic processing of a borrelial protein required for cell fission and infectivity, BB0323, is impaired in BbhtrA mutants grown at 37°C, which likely contributed to their inability to survive in a mammalian host.
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The evolving story of Borrelia burgdorferi sensu lato transmission in Europe
TL;DR: In this article , the authors present the current knowledge about the pathogens including their astonishing ability to overcome various host immune responses, regarding the main vector in Europe Ixodes ricinus, and the disease caused by Borreliae.
Journal ArticleDOI
Lipoproteome screening of the Lyme disease agent identifies inhibitors of antibody-mediated complement killing
Michael J. Pereira,Beau Wager,Ryan J. Garrigues,Eva Gerlach,Joshua D. Quinn,Alexander S. Dowdell,Marcia S. Osburne,Wolfram R. Zückert,Peter Kraiczy,Brandon L. Garcia,John M. Leong +10 more
TL;DR: This work generated a platform to rapidly identify targets of B. burgdorferi surface lipoproteins and identified two paralogs that confer resistance to antibody-initiated complement killing that may promote survival in immunocompetent hosts.
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The Lyme disease spirochete can hijack the host immune system for extravasation from the microvasculature
TL;DR: In this paper, the authors studied the mechanism by which the spirochete Borrelia burgdorferi can breach the blood vessel wall to reach distant tissues and found that host neutrophils are involved in the production of specific cytokines that activate the endothelium.
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TL;DR: A treponema-like spirochete was detected in and isolated from adult Ixodes dammini, the incriminated tick vector of Lyme disease, and it is suggested that the newly discovered spiroChete is involved in the etiology of Lyme Disease.
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