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  1. Article: Broadly conserved FlgV controls flagellar assembly and

    Zamba-Campero, Maxime / Soliman, Daniel / Yu, Huaxin / Lasseter, Amanda G / Chang, Yuen-Yan / Liu, Jun / Aravind, L / Jewett, Mollie W / Storz, Gisela / Adams, Philip P

    bioRxiv : the preprint server for biology

    2024  

    Abstract: Flagella propel pathogens through their environments yet are expensive to synthesize and are immunogenic. Thus, complex hierarchical regulatory networks control flagellar gene expression. Spirochetes are highly motile bacteria, but peculiarly in the Lyme ...

    Abstract Flagella propel pathogens through their environments yet are expensive to synthesize and are immunogenic. Thus, complex hierarchical regulatory networks control flagellar gene expression. Spirochetes are highly motile bacteria, but peculiarly in the Lyme spirochete
    Language English
    Publishing date 2024-01-09
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2024.01.09.574855
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Structural evolution of an immune evasion determinant shapes pathogen host tropism.

    Marcinkiewicz, Ashley L / Brangulis, Kalvis / Dupuis, Alan P / Hart, Thomas M / Zamba-Campero, Maxime / Nowak, Tristan A / Stout, Jessica L / Akopjana, Inara / Kazaks, Andris / Bogans, Janis / Ciota, Alexander T / Kraiczy, Peter / Kolokotronis, Sergios-Orestis / Lin, Yi-Pin

    Proceedings of the National Academy of Sciences of the United States of America

    2023  Volume 120, Issue 27, Page(s) e2301549120

    Abstract: Modern infectious disease outbreaks often involve changes in host tropism, the preferential adaptation of pathogens to specific hosts. The Lyme disease-causing ... ...

    Abstract Modern infectious disease outbreaks often involve changes in host tropism, the preferential adaptation of pathogens to specific hosts. The Lyme disease-causing bacterium
    MeSH term(s) Animals ; Humans ; Immune Evasion/genetics ; Phylogeny ; Viral Tropism ; Lyme Disease/microbiology ; Borrelia burgdorferi ; Bacterial Proteins/metabolism ; Complement Factor H/genetics ; Complement Factor H/metabolism ; Complement System Proteins/genetics ; Membrane Proteins/metabolism
    Chemical Substances Bacterial Proteins ; Complement Factor H (80295-65-4) ; Complement System Proteins (9007-36-7) ; Membrane Proteins
    Language English
    Publishing date 2023-06-26
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, Non-U.S. Gov't
    ZDB-ID 209104-5
    ISSN 1091-6490 ; 0027-8424
    ISSN (online) 1091-6490
    ISSN 0027-8424
    DOI 10.1073/pnas.2301549120
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Blood treatment of Lyme borreliae demonstrates the mechanism of CspZ-mediated complement evasion to promote systemic infection in vertebrate hosts.

    Marcinkiewicz, Ashley L / Dupuis, Alan P / Zamba-Campero, Maxime / Nowak, Nancy / Kraiczy, Peter / Ram, Sanjay / Kramer, Laura D / Lin, Yi-Pin

    Cellular microbiology

    2019  Volume 21, Issue 2, Page(s) e12998

    Abstract: Lyme disease, caused by the spirochete Borrelia burgdorferi, is the most common vector-borne disease in the United States and Europe. The spirochetes are transmitted from mammalian and avian reservoir hosts to humans via ticks. Following tick bites, ... ...

    Abstract Lyme disease, caused by the spirochete Borrelia burgdorferi, is the most common vector-borne disease in the United States and Europe. The spirochetes are transmitted from mammalian and avian reservoir hosts to humans via ticks. Following tick bites, spirochetes colonize the host skin and then disseminate haematogenously to various organs, a process that requires this pathogen to evade host complement, an innate immune defence system. CspZ, a spirochete surface protein, facilitates resistance to complement-mediated killing in vitro by binding to the complement regulator, factor H (FH). Low expression levels of CspZ in spirochetes cultivated in vitro or during initiation of infection in vivo have been a major hurdle in delineating the role of this protein in pathogenesis. Here, we show that treatment of B. burgdorferi with human blood induces CspZ production and enhances resistance to complement. By contrast, a cspZ-deficient mutant and a strain that expressed an FH-nonbinding CspZ variant were impaired in their ability to cause bacteraemia and colonize tissues of mice or quail; virulence of these mutants was however restored in complement C3-deficient mice. These novel findings suggest that FH binding to CspZ facilitates B. burgdorferi complement evasion in vivo and promotes systemic infection in vertebrate hosts.
    MeSH term(s) Animals ; Bacterial Proteins/genetics ; Bacterial Proteins/metabolism ; Borrelia burgdorferi/immunology ; Borrelia burgdorferi/pathogenicity ; Complement C3/genetics ; Complement C3/immunology ; Complement Factor H/immunology ; Complement Factor H/metabolism ; Coturnix ; Humans ; Ixodes/microbiology ; Lyme Disease/immunology ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Knockout
    Chemical Substances Bacterial Proteins ; CFH protein, human ; Complement C3 ; Membrane Proteins ; Complement Factor H (80295-65-4)
    Language English
    Publishing date 2019-01-07
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 1468320-9
    ISSN 1462-5822 ; 1462-5814
    ISSN (online) 1462-5822
    ISSN 1462-5814
    DOI 10.1111/cmi.12998
    Database MEDical Literature Analysis and Retrieval System OnLINE

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