scholarly journals MyD88 Deficiency Enhances Acquisition and Transmission of Borrelia burgdorferi by Ixodes scapularis Ticks

2006 ◽  
Vol 74 (4) ◽  
pp. 2154-2160 ◽  
Author(s):  
Linda K. Bockenstedt ◽  
Nengyin Liu ◽  
Ira Schwartz ◽  
Durland Fish
Keyword(s):  
Borrelia Burgdorferi ◽  
Ixodes Scapularis ◽  
Innate Immune ◽  
Wild Type ◽  
Effector Functions ◽  
Tick Vector ◽  
Inoculation Site ◽  
High Virulence ◽  
The Mean ◽  
Pathogen Burden

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.

Defining Plasmids Required by Borrelia burgdorferi for Colonization of Tick Vector Ixodes scapularis (Acari: Ixodidae)

2005 ◽  
Vol 42 (4) ◽  
pp. 676-684 ◽  
Author(s):  
Dorothee Grimm ◽  
Kit Tilly ◽  
Dawn M. Bueschel ◽  
Mark A. Fisher ◽  
Paul F. Policastro ◽  
...  
Keyword(s):  
Borrelia Burgdorferi ◽  
Ixodes Scapularis ◽  
Tick Vector

scholarly journals The luxS Gene Is Not Required for Borrelia burgdorferi Tick Colonization, Transmission to a Mammalian Host, or Induction of Disease

2004 ◽  
Vol 72 (8) ◽  
pp. 4864-4867 ◽  
Author(s):  
Jon S. Blevins ◽  
Andrew T. Revel ◽  
Melissa J. Caimano ◽  
Xiaofeng F. Yang ◽  
James A. Richardson ◽  
...  
Keyword(s):  
Borrelia Burgdorferi ◽  
Ixodes Scapularis ◽  
Mammalian Host ◽  
Luxs Gene ◽  
Wild Type ◽  
Molting Process

ABSTRACT luxS mutants of Borrelia burgdorferi strain 297 naturally colonized their arthropod (Ixodes scapularis) vector, were maintained in ticks throughout the molting process (larvae to nymphs), were tick transmitted to uninfected mice, and elicited histopathology in mice indistinguishable from that induced by wild-type B. burgdorferi.

scholarly journals The unusual cell wall of the Lyme disease spirochaete Borrelia burgdorferi is shaped by a tick sugar

2021 ◽  
Vol 6 (12) ◽  
pp. 1583-1592
Author(s):  
Tanner G. DeHart ◽  
Mara R. Kushelman ◽  
Sherry B. Hildreth ◽  
Richard F. Helm ◽  
Brandon L. Jutras
Keyword(s):  
Cell Wall ◽  
Lyme Disease ◽  
Borrelia Burgdorferi ◽  
Cell Walls ◽  
Structural Strength ◽  
Cell Envelope ◽  
Wild Type ◽  
Tick Vector ◽  
Cell Wall Alteration ◽  
Main Component

AbstractPeptidoglycan—a mesh sac of glycans that are linked by peptides—is the main component of bacterial cell walls. Peptidoglycan provides structural strength, protects cells from osmotic pressure and contributes to shape. All bacterial glycans are repeating disaccharides of N-acetylglucosamine (GlcNAc) β-(1–4)-linked to N-acetylmuramic acid (MurNAc). Borrelia burgdorferi, the tick-borne Lyme disease pathogen, produces glycan chains in which MurNAc is occasionally replaced with an unknown sugar. Nuclear magnetic resonance, liquid chromatography–mass spectroscopy and genetic analyses show that B. burgdorferi produces glycans that contain GlcNAc–GlcNAc. This unusual disaccharide is chitobiose, a component of its chitinous tick vector. Mutant bacteria that are auxotrophic for chitobiose have altered morphology, reduced motility and cell envelope defects that probably result from producing peptidoglycan that is stiffer than that in wild-type bacteria. We propose that the peptidoglycan of B. burgdorferi probably evolved by adaptation to obligate parasitization of a tick vector, resulting in a biophysical cell-wall alteration to withstand the atypical torque associated with twisting motility.

scholarly journals Isolation of Borrelia burgdorferi from saliva of the tick vector, Ixodes scapularis.

1994 ◽  
Vol 32 (3) ◽  
pp. 755-758 ◽  
Author(s):  
C Ewing ◽  
A Scorpio ◽  
D R Nelson ◽  
T N Mather
Keyword(s):  
Borrelia Burgdorferi ◽  
Ixodes Scapularis ◽  
Tick Vector

scholarly journals Characterization of Stress and Innate Immunity Resistance of Wild-Type and Δp66 Borrelia burgdorferi

2017 ◽  
Vol 86 (2) ◽  
Author(s):  
Michael W. Curtis ◽  
Beth L. Hahn ◽  
Kai Zhang ◽  
Chunhao Li ◽  
Richard T. Robinson ◽  
...  
Keyword(s):  
Borrelia Burgdorferi ◽  
Antimicrobial Peptide ◽  
Membrane Integrity ◽  
The United States ◽  
Laboratory Model ◽  
Wild Type ◽  
Content Type ◽  
Inoculation Site

ABSTRACTBorrelia burgdorferiis a causative agent of Lyme disease, the most common arthropod-borne disease in the United States.B. burgdorferievades host immune defenses to establish a persistent, disseminated infection. Previous work showed that P66-deficientB. burgdorferi(Δp66) is cleared quickly after inoculation in mice. We demonstrate that the Δp66strain is rapidly cleared from the skin inoculation site prior to dissemination. The rapid clearance of Δp66bacteria is not due to inherent defects in multiple properties that might affect infectivity: bacterial outer membrane integrity, motility, chemotactic response, or nutrient acquisition. This led us to the hypothesis that P66 has a role in mouse cathelicidin-related antimicrobial peptide (mCRAMP; a major skin antimicrobial peptide) and/or neutrophil evasion. Neither wild-type (WT) nor Δp66 B. burgdorferiwas susceptible to mCRAMP. To examine the role of neutrophil evasion, we administered neutrophil-depleting antibody anti-Ly6G (1A8) to C3H/HeN mice and subsequently monitored the course ofB. burgdorferiinfection. Δp66mutants were unable to establish infection in neutrophil-depleted mice, suggesting that the important role of P66 during early infection is through another mechanism. Neutrophil depletion did not affect WTB. burgdorferibacterial burdens in the skin (inoculation site), ear, heart, or tibiotarsal joint at early time points postinoculation. This was unexpected given that priorin vitrostudies demonstrated neutrophils phagocytose and killB. burgdorferi. These data, together with our previous work, suggest that despite thein vitroability of host innate defenses to killB. burgdorferi, individual innate immune mechanisms have limited contributions to controlling earlyB. burgdorferiinfection in the laboratory model used.

scholarly journals Infectivity of the Highly Transformable BBE02− lp56− Mutant of Borrelia burgdorferi, the Lyme Disease Spirochete, via Ticks

2006 ◽  
Vol 74 (6) ◽  
pp. 3678-3681 ◽  
Author(s):  
Mary B. Jacobs ◽  
Steven J. Norris ◽  
Kathrine M. Phillippi-Falkenstein ◽  
Mario T. Philipp
Keyword(s):  
Lyme Disease ◽  
Borrelia Burgdorferi ◽  
Ixodes Scapularis ◽  
Shuttle Vector ◽  
Lower Number ◽  
Linear Plasmid ◽  
Wild Type ◽  
Gene Encoding ◽  
Restriction Modification ◽  
Feeding Tick

ABSTRACT Infectious Borrelia burgdorferi strains that have increased transformability with the shuttle vector pBSV2 were recently constructed by inactivating the gene encoding BBE02, a putative restriction-modification gene product expressed by the linear plasmid lp25 (Kawabata et al., Infect. Immun. 72:7147-7154, 2004). The absence of the linear plasmid lp56, which carries another putative restriction-modification gene, further enhanced transformation rates. The infectivity of these mutants was assessed previously in mice that were inoculated with needle and syringe and was found to be equivalent to that of wild-type spirochetes. Here we examined the infectivity of spirochetes to ticks after capillary inoculation of Ixodes scapularis nymphs and the subsequent spirochetal infectivity to mice via ticks by using B. burgdorferi B31 clonal isolates lacking lp56 and/or BBE02. The absence of lp56 (but not BBE02) correlated with a lower number of spirochetes in ticks after feeding on mice; this plasmid thus may play a role, albeit not an essential one, in supporting spirochetal survival in the feeding tick. Importantly, however, the absence of lp56 and BBE02 did not detectably influence infectivity to mice via ticks.

DURATION OF BORRELIA BURGDORFERI INFECTIVITY IN WHITE-FOOTED MICE FOR THE TICK VECTOR IXODES SCAPULARIS UNDER LABORATORY AND FIELD CONDITIONS IN ONTARIO

1997 ◽  
Vol 33 (4) ◽  
pp. 766-775 ◽  
Author(s):  
L. Robbin Lindsay ◽  
Ian K. Barker ◽  
Gordon A. Surgeoner ◽  
Scott A. McEwen ◽  
G. Douglas Campbell
Keyword(s):  
Borrelia Burgdorferi ◽  
Ixodes Scapularis ◽  
Field Conditions ◽  
Tick Vector

The effect of infection with Lyme disease spirochetes (Borrelia burgdorferi) on the phototaxis, activity, and questing height of the tick vector Ixodes scapularis

Parasitology ◽  
1996 ◽  
Vol 113 (2) ◽  
pp. 97-103 ◽  
Author(s):  
H. Lefcort ◽  
L. A. Durden
Keyword(s):  
Lyme Disease ◽  
Borrelia Burgdorferi ◽  
Kin Selection ◽  
Ixodes Scapularis ◽  
Bacterial Pathogen ◽  
Pathogen Transmission ◽  
Ecological Effects ◽  
Infected Tick ◽  
Tick Vector ◽  
Tick Vectors

SUMMARYLittle is known about the effects of infection with Borrelia burgdorferi, the bacterium that causes Lyme disease, on its tick vectors. The purpose of this study was to determine the behavioural and ecological effects of infection by the bacterium in nymphal and adult black-legged (Ixodes scapularis) ticks. We found that the effects of infection were more pronounced in adults than in nymphs. Compared to uninfected adults, infected adults were less able to overcome physical obstacles, avoided vertical surfaces, were less active and quested at lower heights. Infected nymphs showed increased phototaxis and attraction to vertical surfaces. Infected nymphs also showed trends toward increased questing height and a greater tendency to overcome physical obstacles although these trends were not statistically significant. These altered behaviours in an infected tick may affect survival or pathogen transmission and may reflect kin selection in the bacterial pathogen.

scholarly journals Viable Borrelia burgdorferi Enhances Interleukin-10 Production and Suppresses Activation of Murine Macrophages

2007 ◽  
Vol 76 (3) ◽  
pp. 1153-1162 ◽  
Author(s):  
John J. Lazarus ◽  
Maria A. Kay ◽  
Akisha L. McCarter ◽  
R. Mark Wooten
Keyword(s):  
Borrelia Burgdorferi ◽  
Immune Responses ◽  
Culture Medium ◽  
Interleukin 10 ◽  
Innate Immune ◽  
Innate Immune Responses ◽  
Wild Type ◽  
Adaptive Immune

ABSTRACT Although it is capable of eliciting strong innate and adaptive immune responses, Borrelia burgdorferi often evades immune clearance through largely unknown mechanisms. Our previous studies determined that infected interlukin-10−/− (IL-10−/−) mice show significantly lower B. burgdorferi levels than wild-type (B6) mice and that IL-10 inhibits innate immune responses critical for controlling B. burgdorferi infection. To determine whether virulent B. burgdorferi preferentially enhances IL-10 production, we developed an in vitro coculture medium (RPMI.B) in which both B. burgdorferi and primary macrophages (Mφs) remain viable. B. burgdorferi grew at similar rates and was able to regulate expression of immunoreactive proteins with similar kinetics in RPMI.B and in traditional BSK medium; in contrast, B. burgdorferi cultured in conventional tissue culture medium (RPMI) rapidly lost viability. Coculture of viable B. burgdorferi in RPMI.B with Mφs resulted in more rapid and significant increases in IL-10 transcripts and secreted proteins than coculture with nonviable B. burgdorferi in RPMI, which corresponded with decreased production of proinflammatory cytokines. Addition of live B. burgdorferi to Mφs in RPMI.B also elicited substantially higher IL-10 levels than heat-killed bacteria elicited, confirming that increased IL-10 production was not inherent to coculture in RPMI.B. Transfer of supernatants from B. burgdorferi-stimulated Mφs into naïve Mφ cultures resulted in suppressed activation upon subsequent stimulation with different bacterial agonists, and this suppression was obviated by IL-10-specific antibody. In vivo analyses determined that murine skin samples exhibited substantial upregulation of IL-10 within 24 h of injection of B. burgdorferi. Together, these results suggest that viable B. burgdorferi can suppress early Mφ responses during infection by causing increased release of IL-10.

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