Open Access

REVIEW

Activation of innate host defense mechanisms by Borrelia

Anneleen Berende^1,3, Marije Oosting^1,2, Bart-Jan Kullberg^1,2, Mihai G. Netea^1,2, Leo A. B. Joosten^1,2

1 Department of Medicine, Radboud University Nijmegen Medical Center, Nijmegen
2 Nijmegen Institute for Infection, Inflammation and Immunity (N4i)
3 Department of Internal Medicine, Jeroen Bosch Hospital, ‘s Hertogenbosch, The Netherlands

* Corresponding Author: L.A.B. Joosten,

European Cytokine Network 2010, 21(1), 7-18. https://doi.org/10.1684/ecn.2009.0179

Accepted 15 September 2009;

Abstract

Borrelia is the causative agent of Lyme disease, a widespread disease with important health conse-quences. Immune-mediated mechanisms are believed to play a major role in both host defense and in late com-plications of Lyme disease. Recognition of Borrelia and the initial activation of the innate immune system are important for host defense, as well as modulation of adaptive responses. Several classes of pattern recognition receptors (PRRs) have been suggested to be involved in the recognition of Borrelia: Toll-like receptors (TLRs), NOD-like receptors (NLRs) and C-type lectin receptors (CLRs). TLR2 has been found to be the most important receptor of the TLRs. The intracellular receptor NOD2, a member of the NLRs, might also play an important role in recognition. Mannose receptor is also involved in Borrelia recognition, but little is known about other CLRs such as dectin-1. After PRRs have recognized Borrelia, a signaling cascade is induced that leads to tran-scription of NF-κB, resulting in the production of pro-inflammatory cytokines. Understanding these pathways provides not only a better insight into the pathogenesis, but also provides potential, novel, therapeutic targets during active disease or post-infection complications.

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Keywords

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