Borrelia burgdorferi inhibits human neutrophil functions

Hartiala, Pauliina; Hytönen, Jukka; Suhonen, Juha; Leppäranta, Outi; Tuominen-Gustafsson, Helena; Viljanen, Matti K.

doi:10.1016/j.micinf.2007.10.004

Cited by 32 publications

(29 citation statements)

References 27 publications

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“…This could be due to either the failure of the mutant to be transmitted from the tick vector to mice or the failure of the mutant to survive and establish an infection in mice after the completion of transmission. Bacterial chemotaxis is likely required for the early dissemination and invasion after initial deposition to evade incoming host innate immune cells, such as neutrophils (21). Consistently, the kinetics study of infection using needle inoculation revealed that the mutant cells were removed from the initial inoculation site within 72 h (Fig.…”

Section: Discussionsupporting

confidence: 62%

Borrelia burgdorferi Needs Chemotaxis To Establish Infection in Mammals and To Accomplish Its Enzootic Cycle

et al. 2012

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ABSTRACTBorrelia burgdorferi, the causative agent of Lyme disease, can be recovered from different organs of infected animals and patients, indicating that the spirochete is very invasive. Motility and chemotaxis contribute to the invasiveness ofB. burgdorferiand play important roles in the process of the disease. Recent reports have shown that motility is required for establishing infection in mammals. However, the role of chemotaxis in virulence remains elusive. Our previous studies showed thatcheA2, a gene encoding a histidine kinase, is essential for the chemotaxis ofB. burgdorferi. In this report, thecheA2gene was inactivated in a low-passage-number virulent strain ofB. burgdorferi. In vitroanalyses (microscopic observations, computer-based bacterial tracking analysis, swarm plate assays, and capillary tube assays) showed that thecheA2mutant failed to reverse and constantly ran in one direction; the mutant was nonchemotactic to attractants. Mouse needle infection studies showed that thecheA2mutant failed to infect either immunocompetent or immunodeficient mice and was quickly eliminated from the initial inoculation sites. Tick-mouse infection studies revealed that although the mutant was able to survive in ticks, it failed to establish a new infection in mice via tick bites. The altered phenotypes were completely restored when the mutant was complemented. Collectively, these data demonstrate thatB. burgdorferineeds chemotaxis to establish mammalian infection and to accomplish its natural enzootic cycle.

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Section: Discussionsupporting

confidence: 62%

Borrelia burgdorferi Needs Chemotaxis To Establish Infection in Mammals and To Accomplish Its Enzootic Cycle

et al. 2012

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“…The surface proteins of a spirochete affect significant stages of the immunological response: OspA inhibits the spirochetes' phagocytosis and an oxygen explosion in neutrophils especially at the low concentration of a complement, which substantially simplifies the survival and the dissemination of bacteria. The spirochetes can bind with the receptor cells molecules of a host and the extracellular matrix as integrins, glycoproteins, and proteoglycans (Hartiala, et al, 2008). The antibodies IgG anti-B.…”

Section: The Antigen Proteins B Burgdorferi Diagnostically Significantmentioning

confidence: 99%

“…That kind of capability does not have B. garinii which are sensitive on the complement's effect (Krajczy, et al, 2001;Suchonen, et al, 2002;Zajkowska, et al, 2006c). Serum resistance of B. burgdorferi B31 is mainly associated witch CRASP-1 and mediated by binding of complement regulator factor H. OspA and OspC do not bind factor H (Hartiala, et al, 2008). Regardless of the way on which the activation of the complement occurs, the development of the membrane -attack complex (MAC) is a key stage.…”

Section: The Complement Systemmentioning

confidence: 99%

The Serology Diagnostic Schemes in Borrelia burgdorferi Sensu Lato Infections – Significance in Clinical Practice

Tokarska-Rodak¹,

Kozioł-Montewka²

2012

Lyme Disease

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“…Nevertheless, B. burgdorferi s.l. developed mechanisms to escape neutrophil defenses by inhibiting their chemotaxis induced by fMLF activation and their phagocytosis and oxidative burst via OspB (10). Moreover, the swift movements of Borrelia spirochetes allow them to escape neutrophils (11).…”

mentioning

confidence: 99%

Neutrophil Extracellular Traps Entrap and KillBorrelia burgdorferiSensu Stricto Spirochetes and Are Not Affected byIxodes ricinusTick Saliva

Menten-Dedoyart

Faccinetto

Golovchenko

et al. 2012

The Journal of Immunology

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Lyme disease is caused by spirochetes of the Borrelia burgdorferi sensu lato complex. They are transmitted mainly by Ixodes ricinus ticks. After a few hours of infestation, neutrophils massively infiltrate the bite site. They can kill Borrelia via phagocytosis, oxidative burst, and hydrolytic enzymes. However, factors in tick saliva promote propagation of the bacteria in the host even in the presence of a large number of neutrophils. The neutrophil extracellular trap (NET) consists in the extrusion of the neutrophil’s own DNA, forming traps that can retain and kill bacteria. The production of reactive oxygen species is apparently associated with the onset of NETs (NETosis). In this article, we describe NET formation at the tick bite site in vivo in mice. We show that Borrelia burgdorferi sensu stricto spirochetes become trapped and killed by NETs in humans and that the bacteria do not seem to release significant nucleases to evade this process. Saliva from I. ricinus did not affect NET formation by human neutrophils or its stability. However, it greatly decreased neutrophil reactive oxygen species production, suggesting that a strong decrease of hydrogen peroxide does not affect NET formation. Finally, round bodies trapped in NETs were observed, some of them staining as live bacteria. This observation could help contribute to a better understanding of the early steps of Borrelia invasion and erythema migrans formation after tick bite.

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Borrelia burgdorferi inhibits human neutrophil functions

Cited by 32 publications

References 27 publications

Borrelia burgdorferi Needs Chemotaxis To Establish Infection in Mammals and To Accomplish Its Enzootic Cycle

Borrelia burgdorferi Needs Chemotaxis To Establish Infection in Mammals and To Accomplish Its Enzootic Cycle

The Serology Diagnostic Schemes in Borrelia burgdorferi Sensu Lato Infections – Significance in Clinical Practice

Neutrophil Extracellular Traps Entrap and KillBorrelia burgdorferiSensu Stricto Spirochetes and Are Not Affected byIxodes ricinusTick Saliva

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