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  • 1
    Online Resource
    Online Resource
    Marginal Zone B-Cell Depletion Impairs Murine Host Defense against Borrelia burgdorferi Infection
    American Society for Microbiology ; 2007
    In:  Infection and Immunity Vol. 75, No. 7 ( 2007-07), p. 3354-3360
    Details
    In: Infection and Immunity, American Society for Microbiology, Vol. 75, No. 7 ( 2007-07), p. 3354-3360
    Abstract: Marginal zone B (MZB) cells are a B-cell subset that produces T-cell-independent antibodies to blood-borne antigens. In this study, we examined the effects of MZB cell depletion on the immune response to the Lyme disease spirochete Borrelia burgdorferi , an extracellular pathogen for which T-cell-independent antibody is an important host defense. MZB cell depletion of C3H/HeJ mice using monoclonal antibody to LFA-1 and α 4 β 1 integrins reduced B. burgdorferi -specific immunoglobulin M (IgM) titers, enhanced pathogen burden, and led to more severe arthritis assessed within the first 2 weeks of infection. In addition, MZB cell-depleted mice had reduced levels of B. burgdorferi -specific IgG, which correlated with diminished splenic CD4 + T-cell-activation, proliferation, and cytokine production. Passive transfer of immune mouse serum from infected control mice into infected MZB cell-depleted mice reduced pathogen burden but did not alter the expression of T-cell activation markers on splenic CD4 + T cells. These findings demonstrate that MZB cells not only are a source of pathogen-specific IgM important for limiting spirochete burden and pathology but also play a prominent role in the priming of splenic T-cell responses to a blood-borne pathogen.
    Type of Medium: Online Resource
    ISSN: 0019-9567 , 1098-5522
    URL: Article
    DOI: 10.1128/IAI.00422-07
    RVK:
    XA 10000
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2007
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  • 2
    Online Resource
    Online Resource
    MyD88 Deficiency Enhances Acquisition and Transmission of Borrelia burgdorferi by Ixodes scapularis Ticks
    American Society for Microbiology ; 2006
    In:  Infection and Immunity Vol. 74, No. 4 ( 2006-04), p. 2154-2160
    Details
    In: Infection and Immunity, American Society for Microbiology, Vol. 74, No. 4 ( 2006-04), p. 2154-2160
    Abstract: Borrelia burgdorferi strains exhibit various degrees of infectivity and pathogenicity in mammals, which may be due to their relative ability to evade initial host immunity. Innate immune cells recognize B. burgdorferi by Toll-like receptors (TLRs) that use the intracellular molecule MyD88 to mediate effector functions. To determine whether impaired TLR signaling enhances Ixodes scapularis acquisition of B. burgdorferi , we fed nymphs on wild-type (WT) and MyD88 −/− mice previously infected with two clinical isolates of B. burgdorferi , BL206, a high-virulence strain, and B348, an attenuated strain. Seventy-three percent of the nymphs that fed on BL206-infected WT mice and 40% of the nymphs that fed on B348-infected WT mice acquired B. burgdorferi , whereas 100% of the nymphs that fed on MyD88 −/− mice became infected, irrespective of B. burgdorferi strain. Ticks that acquired infection after feeding on MyD88 −/− mice harbored more spirochetes than those that fed on WT mice, as assessed by quantitative PCR for B. burgdorferi DNA. Vector transmission of BL206 and B348 was also enhanced when MyD88 −/− mice were the blood meal hosts, with the mean pathogen burden at the skin inoculation site significantly higher than levels in WT mice. These results show that the absence of MyD88 facilitates passage of both low- and high-infectivity B. burgdorferi strains between the tick vector and the mammal and enhances the infectivity of a low-infectivity B. burgdorferi strain.
    Type of Medium: Online Resource
    ISSN: 0019-9567 , 1098-5522
    URL: Article
    DOI: 10.1128/IAI.74.4.2154-2160.2006
    RVK:
    XA 10000
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2006
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  • 3
    Online Resource
    Online Resource
    Natural Antibody Affects Survival of the Spirochete Borrelia burgdorferi within Feeding Ticks
    American Society for Microbiology ; 2001
    In:  Infection and Immunity Vol. 69, No. 10 ( 2001-10), p. 6456-6462
    Details
    In: Infection and Immunity, American Society for Microbiology, Vol. 69, No. 10 ( 2001-10), p. 6456-6462
    Abstract: Natural antibodies are those immunoglobulin molecules found in mammalian serum that arise in the absence of exposure to environmental pathogens and may comprise an early host defense against invading pathogens. The spirochete Borrelia burgdorferi first encounters natural antibodies when its arthropod vector, Ixodes scapularis , begins feeding on a mammalian host. Natural antibodies may therefore have an impact on pathogens within blood-sucking vectors, prior to pathogen transmission to the mammal. In this study, we investigated whether natural antibodies influenced the number and/or phenotype of B. burgdorferi organisms within feeding I. scapularis nymphs. Using a competitive PCR, we found that ticks ingesting a blood meal from B-cell-deficient mice, which lack all immunoglobulins, contained fivefold more spirochete DNA than ticks feeding on control mice. Spirochete DNA levels could be reduced to that of controls with passive transfer of normal mouse serum or polyclonal immunoglobulin M (IgM), but not IgG, into B-cell-deficient mice prior to placement of infected ticks. At 48 h of tick feeding, 90% of spirochetes within salivary glands of ticks removed from B-cell-deficient mice were found by confocal immunofluorescence microscopy to express outer surface protein A (OspA), compared to only 5% of salivary gland spirochetes from ticks detached from control mice. Taken together, these results show that ingestion of natural antibodies limits the spirochete burden within feeding ticks. Because OspA is normally downregulated when spirochetes moved from the tick midgut to the salivary gland, our findings suggest that OspA-expressing midgut spirochetes may be particularly susceptible to the borrelicidal effects of these molecules.
    Type of Medium: Online Resource
    ISSN: 0019-9567 , 1098-5522
    URL: Article
    DOI: 10.1128/IAI.69.10.6456-6462.2001
    RVK:
    XA 10000
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2001
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  • 4
    Online Resource
    Online Resource
    Modulation of Murine Lyme Borreliosis by Interruption of the B7/CD28 T-Cell Costimulatory Pathway
    American Society for Microbiology ; 1998
    In:  Infection and Immunity Vol. 66, No. 1 ( 1998-01), p. 266-271
    Details
    In: Infection and Immunity, American Society for Microbiology, Vol. 66, No. 1 ( 1998-01), p. 266-271
    Abstract: Recent studies have implicated cytokines associated with Th2 cells in the genetic resistance to murine Lyme borreliosis. Because the B7/CD28 costimulatory pathway has been shown to influence the differentiation of Th-cell subsets, we investigated the contribution of the B7 molecules CD80 and CD86 to the Th2 cytokine profile and development of arthritis in BALB/c mice infected with Borrelia burgdorferi . Effective blockade of CD86/CD28 interaction was demonstrated by elimination of interleukin 4 (IL-4) and upregulation of gamma interferon (IFN-γ) responses by B. burgdorferi -specific T cells and by reduction of B. burgdorferi -specific immunoglobulin G. Despite the shift toward a Th1 cytokine pattern, which others have associated with disease susceptibility, the severity of arthritis was unchanged. Moreover, combined CD80/CD86 blockade by using anti-CD80 and anti-CD86 monoclonal antibodies or CTLA-4Ig enhanced IFN-γ production over that seen with CD86 blockade alone, yet augmentation of this Th1-associated cytokine did not enhance disease. These results demonstrate that IL-4 production by T cells in B. burgdorferi -infected BALB/c mice is dependent upon CD86/CD28 interaction and that this cytokine does not contribute significantly to host resistance to the development of arthritis. In addition, combined CD80/CD86 blockade resulted in preferential expansion of IFN-γ-producing T cells in B. burgdorferi infection, suggesting that costimulatory pathways other than B7/CD28 may contribute to T-cell activation during continuous antigen stimulation. These studies may provide insight into the role of the B7/CD28 pathway in other infectious and autoimmune diseases in which deviation of Th cell immune responses occurs and antigen is persistently present.
    Type of Medium: Online Resource
    ISSN: 0019-9567 , 1098-5522
    URL: Article
    DOI: 10.1128/IAI.66.1.266-271.1998
    RVK:
    XA 10000
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 1998
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  • 5
    Online Resource
    Online Resource
    The Caspase 1 Inflammasome Is Not Required for Control of Murine Lyme Borreliosis
    American Society for Microbiology ; 2009
    In:  Infection and Immunity Vol. 77, No. 8 ( 2009-08), p. 3320-3327
    Details
    In: Infection and Immunity, American Society for Microbiology, Vol. 77, No. 8 ( 2009-08), p. 3320-3327
    Abstract: The contribution of the inflammasome to the development of immune responses and disease during infection with the Lyme disease spirochete, Borrelia burgdorferi , is not well defined. Host defense against the spirochete is severely impaired in mice deficient in the adaptor molecule myeloid differentiation antigen 88 (MyD88), which is required not only for Toll-like receptor-mediated responses but also for the production of the proforms of interleukin 1β (IL-1β) and IL-18. These cytokines are released in active forms after cleavage by the inflammasome-associated enzyme caspase 1. To investigate the contribution of the inflammasome to host defense against B. burgdorferi , we examined Lyme borreliosis in mice deficient in either caspase 1 or apoptosis-associated speck-like protein containing a C-terminal caspase recruitment domain (ASC), a molecule upstream of caspase 1 in the inflammasome signaling cascade. We found that caspase 1-deficient mice had a mild transient elevation in pathogen burden and a trend toward an increase in the prevalence of arthritis early in infection, but these differences resolved by day 14 postinfection. Caspase 1 deficiency had no effect on B. burgdorferi -induced humoral immunity, T-cell responses, or the abilities of macrophages to ingest and degrade spirochetes. The absence of the ASC protein had no effect on the control of the spirochete or the development of immune responses and disease. These findings reveal that the caspase 1 inflammasome is not critical to host defense against the extracellular pathogen Borrelia burgdorferi .
    Type of Medium: Online Resource
    ISSN: 0019-9567 , 1098-5522
    URL: Article
    DOI: 10.1128/IAI.00100-09
    RVK:
    XA 10000
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2009
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  • 6
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    Online Resource
    CD4 + T Helper 1 Cells Facilitate Regression of Murine Lyme Carditis
    American Society for Microbiology ; 2001
    In:  Infection and Immunity Vol. 69, No. 9 ( 2001-09), p. 5264-5269
    Details
    In: Infection and Immunity, American Society for Microbiology, Vol. 69, No. 9 ( 2001-09), p. 5264-5269
    Abstract: Murine Lyme borreliosis, caused by infection with the spirochete Borrelia burgdorferi , results in acute arthritis and carditis that regress as a result of B. burgdorferi -specific immune responses. B. burgdorferi -specific antibodies can attenuate arthritis in mice deficient in both B cells and T cells but have no effect on carditis. Because macrophages comprise the principal immune cell in carditis, T-cell responses that augment cell-mediated immunity may be important for carditis regression. To investigate this hypothesis, we examined the course of Lyme carditis in mice selectively deficient in B cells or αβ T cells. Our results show that carditis regresses in B-cell-deficient B10.A k mice but not in αβ T-cell-deficient mice, independently of the mouse strain background. Despite prominent macrophage infiltrates, hearts from B. burgdorferi -infected αβ T-cell-deficient mice had less mRNA for tumor necrosis factor alpha as measured by reverse transcription-PCR compared to infected control mice. Anti-inflammatory cytokine mRNA levels were equivalent. Adoptive transfer of gamma interferon-secreting CD4 + T cells into infected αβ T-cell-deficient mice promoted carditis resolution. These results show that αβ T cells can promote resolution of murine Lyme carditis and are the first demonstration of a beneficial role for CD4 + T helper 1 cells in this disease.
    Type of Medium: Online Resource
    ISSN: 0019-9567 , 1098-5522
    URL: Article
    DOI: 10.1128/IAI.69.9.5264-5269.2001
    RVK:
    XA 10000
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2001
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  • 7
    Online Resource
    Online Resource
    Myeloid Differentiation Antigen 88 Deficiency Impairs Pathogen Clearance but Does Not Alter Inflammation in Borrelia burgdorferi -Infected Mice
    American Society for Microbiology ; 2004
    In:  Infection and Immunity Vol. 72, No. 6 ( 2004-06), p. 3195-3203
    Details
    In: Infection and Immunity, American Society for Microbiology, Vol. 72, No. 6 ( 2004-06), p. 3195-3203
    Abstract: The spirochete Borrelia burgdorferi causes acute inflammation in mice that resolves with the development of pathogen-specific adaptive immunity. B. burgdorferi lipoproteins activate innate immune cells via Toll-like receptor 2 (TLR2), but TLR2-deficient mice are not resistant to B. burgdorferi -induced disease, suggesting the involvement of other TLRs or non-TLR mechanisms in the induction of acute inflammation. For this study, we used mice that were deficient in the intracellular adapter molecule myeloid differentiation antigen 88 (MyD88), which is required for all TLR-induced inflammatory responses, to determine whether the interruption of this pathway would alter B. burgdorferi -induced disease. Infected MyD88 −/− mice developed carditis and arthritis, similar to the disease in wild-type (WT) mice analyzed at its peak (days 14 and 28) and during regression (day 45). MyD88 −/− macrophages produced tumor necrosis factor alpha only when spirochetes were opsonized, suggesting a role for B. burgdorferi -specific antibody in disease expression. MyD88 −/− mice produced stronger pathogen-specific Th2-dependent immunoglobulin G1 (IgG1) responses than did WT mice, and their IgM titers remained significantly elevated through 90 days of infection. Despite specific antibodies, the pathogen burden was 250-fold higher in MyD88 −/− mice than in WT mice 45 days after infection; by 90 days of infection, the pathogen burden had diminished substantially in MyD88 −/− mice, but it was still elevated compared to that in WT mice. The elevated pathogen burden may be explained in part by the finding that MyD88 −/− peritoneal macrophages could ingest spirochetes but degraded them more slowly than WT macrophages. Our results show that MyD88-dependent signaling pathways are not required for B. burgdorferi -induced inflammation but are necessary for the efficient control of the pathogen burden by phagocytes.
    Type of Medium: Online Resource
    ISSN: 0019-9567 , 1098-5522
    URL: Article
    DOI: 10.1128/IAI.72.6.3195-3203.2004
    RVK:
    XA 10000
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2004
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  • 8
    Online Resource
    Online Resource
    Humoral Immunity Reflects Altered T Helper Cell Bias in Borrelia burgdorferi -Infected γδ T-Cell-Deficient Mice
    American Society for Microbiology ; 2003
    In:  Infection and Immunity Vol. 71, No. 5 ( 2003-05), p. 2938-2940
    Details
    In: Infection and Immunity, American Society for Microbiology, Vol. 71, No. 5 ( 2003-05), p. 2938-2940
    Abstract: In murine Lyme borreliosis, the absence of γδ T lymphocytes augments the T helper cell 2 type humoral response but does not alter disease susceptibility. Arthropod transmission of Borrelia burgdorferi spirochetes results in similar antibody isotypes when γδ T cells are present, suggesting that vector effects can negate γδ T-cell functions in vivo.
    Type of Medium: Online Resource
    ISSN: 0019-9567 , 1098-5522
    URL: Article
    DOI: 10.1128/IAI.71.5.2938-2940.2003
    RVK:
    XA 10000
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2003
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  • 9
    Online Resource
    Online Resource
    Langerhans Cell Deficiency Impairs Ixodes scapularis Suppression of Th1 Responses in Mice
    American Society for Microbiology ; 2009
    In:  Infection and Immunity Vol. 77, No. 5 ( 2009-05), p. 1881-1887
    Details
    In: Infection and Immunity, American Society for Microbiology, Vol. 77, No. 5 ( 2009-05), p. 1881-1887
    Abstract: Ixodes scapularis ticks transmit a number of human pathogens, including the Lyme disease spirochete Borrelia burgdorferi. I. scapularis suppresses host immunity in the skin to promote feeding and systemically skew T-helper (Th)-cell differentiation toward Th2 cells in secondary lymphoid organs. Although components of tick saliva are known to influence Th-cell polarization, the mechanism whereby tick feeding in the skin modulates regional and systemic Th-cell responses is unknown. In this study, the role of the epidermal Langerhans cell (LC) subset of skin dendritic cells in tick-mediated Th1/Th2-cell immunomodulation was assessed. Mice deficient in LCs (Langerin-DTA mice) exhibited enhanced lymph node (LN) concanavalin A (ConA)-induced Th1 responses after tick infestation in comparison to results for uninfested Langerin-DTA or wild-type (WT) mice, whereas effects on Th2-cell production of interleukin 4 were more variable. Nonetheless, the altered T-cell response did not impact tick feeding or refeeding. Gamma interferon production by ConA-stimulated LN cells of both WT and LC-deficient mice was enhanced by as much as fourfold after B. burgdorferi -infected-tick feeding, indicating that immunomodulatory effects of tick saliva were not able to attenuate the Th1 immune responses induced by this pathogen. Taken together, these findings show a requirement for LCs in the tick-mediated attenuation of Th1 responses in regional lymph nodes but not in the spleens of mice and show that the presence of a pathogen can overcome the Th1-inhibitory effects of tick feeding on the host.
    Type of Medium: Online Resource
    ISSN: 0019-9567 , 1098-5522
    URL: Article
    DOI: 10.1128/IAI.00030-09
    RVK:
    XA 10000
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2009
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