The Brilliance of Borrelia: Mechanisms of Host Immune Evasion by Lyme Disease-Causing Spirochetes

Anderson, Cassidy C.; Brissette, Catherine A.

doi:10.3390/pathogens10030281

Cited by 44 publications

(32 citation statements)

References 132 publications

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“…They can persistently infect and survive in their reservoir hosts for prolonged periods of time without causing any signs of a disease in the infected animals. In fact, spirochetes developed numerous strategies to overcome the innate and the adaptive immune response to prevent elimination by the host’s immune system (Hyde 2017 ; Kurokawa et al 2020 ; Lin et al 2020 ; Anderson and Brissette 2021 ). The ~1780 genes in the genome of B. burgdorferi s.s. strain B31 M1 are located on a single linear chromosome (910 kbp) and ~21 linear and circular plasmids (Fraser et al 1997 ; Casjens et al 2000 ; Pal and Fikrig 2003 ; Schwartz et al 2021 ) and can be regulated to respond to environmental changes.…”

Section: Strategies Of B Burgdorferi Sl To Survive In Ticks and Vertebrate Hostsmentioning

confidence: 99%

The evolving story of Borrelia burgdorferi sensu lato transmission in Europe

Steinbrink

Brugger

Margos³

et al. 2022

Parasitol Res

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Beside mosquitoes, ticks are well-known vectors of different human pathogens. In the Northern Hemisphere, Lyme borreliosis (Eurasia, LB) or Lyme disease (North America, LD) is the most commonly occurring vector-borne infectious disease caused by bacteria of the genus Borrelia which are transmitted by hard ticks of the genus Ixodes. The reported incidence of LB in Europe is about 22.6 cases per 100,000 inhabitants annually with a broad range depending on the geographical area analyzed. However, the epidemiological data are largely incomplete, because LB is not notifiable in all European countries. Furthermore, not only differ reporting procedures between countries, there is also variation in case definitions and diagnostic procedures. Lyme borreliosis is caused by several species of the Borrelia (B.) burgdorferi sensu lato (s.l.) complex which are maintained in complex networks including ixodid ticks and different reservoir hosts. Vector and host influence each other and are affected by multiple factors including climate that have a major impact on their habitats and ecology. To classify factors that influence the risk of transmission of B. burgdorferi s.l. to their different vertebrate hosts as well as to humans, we briefly summarize 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. The research shows, that a higher standardization of case definition, diagnostic procedures, and standardized, long-term surveillance systems across Europe is necessary to improve clinical and epidemiological data.

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Section: Strategies Of B Burgdorferi Sl To Survive In Ticks and Vertebrate Hostsmentioning

confidence: 99%

The evolving story of Borrelia burgdorferi sensu lato transmission in Europe

Steinbrink

Brugger

Margos³

et al. 2022

Parasitol Res

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“…At late EC exposure to Bb, we observed the formation of Bb aggregates, but single motile and viable spirochetes were still present in the culture medium. Past studies have suggested that multiple factors can lead to Bb aggregation (Anderson and Brissette, 2021;Sapi et al, 2012;Alban et al, 2000). However, in our assay we determined that this is the result of the high MOI used, since it also occurs when large amounts of spirochetes are cultured in their normal growth medium (data not shown).…”

Section: Discussionmentioning

confidence: 67%

“…Bb can also localize intracellularly in many host cell types, including ECs, from which it can escape clearance and transmigrate transcellularly (Coleman et al, 1995;Tan et al, 2021;Kumar et al, 2015). Moreover, Bb can undergo different morphological transitions, forming for example spherical round bodies and aggregates (Anderson and Brissette, 2021;Sapi et al, 2012). Whether these alternative Bb forms emerge as a result of the harsh in vitro conditions, the multiplicity of infection, or represent a mechanism to evade in vivo host immune responses remains controversial (Murgia and Cinco, 2004;Anderson et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

Borrelia burgdorferi modulates the physical forces and immunity signaling in endothelial cells

Aparicio-Yuste¹,

Muenkel²,

Axarlis³

et al. 2022

iScience

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“…Lyme disease has been demonstrated to destroy germinal centers of lymph nodes during early infection [72, 73, 84, 85]. These germinal centers are a vital structure that produces long-lived immunoglobulin responses through T-cell-dependent interactions [86].…”

Section: Discussionmentioning

confidence: 99%

Lyme Disease IgG N-linked Glycans Contrast the Canonical Inflammatory Signature

Haslund-Gourley

Grauzam

Mehta

et al. 2022

Preprint

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Lyme disease (LD) infection is caused by Borrelia burgdorferi sensu lato. Due to the limited presence of this pathogen in the bloodstream in humans, diagnosis of LD relies on seroconversion. Immunoglobulins produced in response to infection are differentially glycosylated to promote or inhibit downstream inflammatory responses by the immune system. IgG N-glycan responses to LD have not been characterized. In this study, we analyzed IgG N-glycans from cohorts of healthy controls, acute LD patient serum, and serum collected after acute LD patients completed a 2- to 3-week course of antibiotics and convalesced for 70-90 days. Results indicate that during the acute phase of Bb infection, IgG shifts its glycosylation profile to include structures that are not associated with the classic proinflammatory IgG N-glycan signature. This unexpected result is in direct contrast to what is reported for other inflammatory diseases. Furthermore, IgG N-glycans detected during acute LD infection discriminated between control, acute, and treated cohorts with a sensitivity of 75-100% and specificity of 94.7-100%.Author summaryThe causative agent of Lyme disease (LD), Borrelia burgdorferi sensu lato (Bb), is transmitted from an infected Ixodes tick into the human host dermis during the tick’s blood meal. Currently, LD is the most prevalent vector-borne disease in the US, with an estimated 476,000 annual cases. LD diagnostics rely on patient seroconversion against Bb antigens, and these tests cannot distinguish between an acute patient compared to a patient previously treated for LD. With the goal of identifying novel biomarkers associated specifically with LD infections, we analyzed the glycoprotein Immunoglobulin G (IgG) N-glycan signatures from healthy control, acute LD, and a second time point composed of the same LD patients after antibiotic therapy. We found acute LD IgG N-glycan signatures were significantly different from the canonical pro-inflammatory profile associated with most inflammatory diseases. The dramatic shifts observed in the acute LD time point were further altered at the treated time point. IgG N-glycan signature data was employed to discriminate between acute LD and healthy controls. In addition, IgG N-glycan signatures distinguished patients who completed antibiotic therapy from the acute LD timepoint. Our study will contribute to the accurate and prompt treatment of LD patients and reveals a new research avenue of immune dysregulation associated with LD.Graphical Abstract

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The Brilliance of Borrelia: Mechanisms of Host Immune Evasion by Lyme Disease-Causing Spirochetes

Cited by 44 publications

References 132 publications

The evolving story of Borrelia burgdorferi sensu lato transmission in Europe

The evolving story of Borrelia burgdorferi sensu lato transmission in Europe

Borrelia burgdorferi modulates the physical forces and immunity signaling in endothelial cells

Lyme Disease IgG N-linked Glycans Contrast the Canonical Inflammatory Signature

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