Borrelia Burgdorferi Infection in Mice: Aspects of Inflammation and Immune Responses

1994 ◽  
pp. 201-209 ◽  
Author(s):  
Naveed Honarvar ◽  
Elena Böggemeyer ◽  
Chris Galanos ◽  
Manuel Modolell ◽  
Dietmar Vestweber ◽  
...  
Keyword(s):  
Borrelia Burgdorferi ◽  
Immune Responses

scholarly journals Autophagy suppresses host adaptive immune responses toward Borrelia burgdorferi

2016 ◽  
Vol 100 (3) ◽  
pp. 589-598 ◽  
Author(s):  
Kathrin Buffen ◽  
Marije Oosting ◽  
Yang Li ◽  
Thirumala-Devi Kanneganti ◽  
Mihai G. Netea ◽  
...  
Keyword(s):  
Borrelia Burgdorferi ◽  
Immune Responses ◽  
Adaptive Immune Responses ◽  
Adaptive Immune

scholarly journals Coinfection with Borrelia burgdorferi and the Agent of Human Granulocytic Ehrlichiosis Alters Murine Immune Responses, Pathogen Burden, and Severity of Lyme Arthritis

2001 ◽  
Vol 69 (5) ◽  
pp. 3359-3371 ◽  
Author(s):  
Venetta Thomas ◽  
Juan Anguita ◽  
Stephen W. Barthold ◽  
Erol Fikrig
Keyword(s):  
Borrelia Burgdorferi ◽  
Immune Responses ◽  
Dual Infection ◽  
Pathogen Transmission ◽  
Receptor Expression ◽  
Lyme Arthritis ◽  
Bacterial Burden ◽  
Granulocytic Ehrlichiosis ◽  
Human Granulocytic Ehrlichiosis ◽  
Ifn Γ

ABSTRACT Lyme disease and human granulocytic ehrlichiosis (HGE) are tick-borne illnesses caused by Borrelia burgdorferi and the agent of HGE, respectively. We investigated the influence of dual infection with B. burgdorferi and the HGE agent on the course of murine Lyme arthritis and granulocytic ehrlichiosis. Coinfection resulted in increased levels of both pathogens and more severe Lyme arthritis compared with those in mice infected withB. burgdorferi alone. The increase in bacterial burden during dual infection was associated with enhanced acquisition of both organisms by larval ticks that were allowed to engorge upon infected mice. Coinfection also resulted in diminished interleukin-12 (IL-12), gamma interferon (IFN-γ), and tumor necrosis factor alpha levels and elevated IL-6 levels in murine sera. During dual infection, IFN-γ receptor expression on macrophages was also reduced, implying a decrease in phagocyte activation. These results suggest that coinfection of mice with B. burgdorferi and the HGE agent modulates host immune responses, resulting in increased bacterial burden, Lyme arthritis, and pathogen transmission to the vector.

scholarly journals Mice Lacking CD21 and CD35 Proteins Mount Effective Immune Responses against Borrelia burgdorferi Infection

2007 ◽  
Vol 75 (4) ◽  
pp. 2075-2078 ◽  
Author(s):  
Amanda C. Jacobson ◽  
Ying Ma ◽  
James F. Zachary ◽  
Janis J. Weis ◽  
John H. Weis
Keyword(s):  
Borrelia Burgdorferi ◽  
Immune Responses ◽  
Bacterial Infection ◽  
Complement Receptors ◽  
Wild Type ◽  
Specific Antibodies ◽  
Arthritis Severity

ABSTRACT CD21/35−/− mice, deficient in CD21 and CD35 (complement receptors 2 and 1, respectively), were infected with Borrelia burgdorferi to assess the role of these receptors in a chronic bacterial infection. Although CD21/35−/− mice on both C57BL/6 and BALB/c backgrounds produced less B. burgdorferi-specific antibodies than did wild-type mice, spirochete levels and arthritis severity were similar.

scholarly journals A Murine Model of Lyme Disease Demonstrates That Borrelia burgdorferi Colonizes the Dura Mater and Induces Inflammation in the Central Nervous System

2020 ◽  
Author(s):  
Timothy Casselli ◽  
Ali Divan ◽  
Yvonne Tourand ◽  
Heidi L. Pecoraro ◽  
Catherine A. Brissette
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Lyme Disease ◽  
Borrelia Burgdorferi ◽  
Immune Responses ◽  
Inflammatory Cytokines ◽  
Dura Mater ◽  
Brain Parenchyma ◽  
The Central Nervous System ◽  
Effective Models

ABSTRACTLyme disease, which is caused by infection with Borrelia burgdorferi and related species, can lead to inflammatory pathologies affecting the joints, heart, and nervous systems including the central nervous system (CNS). Inbred laboratory mice are effective models for characterizing B. burgdorferi infection kinetics and host immune responses in joints and heart tissues; however, similar studies are lacking in the CNS of these animals. Here we characterize the kinetics of B. burgdorferi colonization and associated immune responses in the CNS of infected C3H mice during early and subacute infection. B. burgdorferi colonized the dura mater following needle or tick challenge, and induced expression of inflammatory cytokines and a robust IFN response as well as histopathological changes. A sterile IFN response in the absence of B. burgdorferi or inflammatory cytokines was unique to the brain parenchyma, and could provide insights into the mechanism of inflammatory CNS pathology associated with this important pathogen.

A DNA vaccine encoding the outer surface protein C from Borrelia burgdorferi is able to induce protective immune responses

2003 ◽  
Vol 5 (11) ◽  
pp. 939-946 ◽  
Author(s):  
Sandra Scheiblhofer ◽  
Richard Weiss ◽  
Hans Dürnberger ◽  
Sven Mostböck ◽  
Michael Breitenbach ◽  
...  
Keyword(s):  
Borrelia Burgdorferi ◽  
Immune Responses ◽  
Dna Vaccine ◽  
Outer Surface ◽  
Protein C ◽  
Surface Protein ◽  
Outer Surface Protein
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