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Infectious Disease Clinics of North... Jun 2008The spirochete Borrelia burgdorferi is a tick-borne obligate parasite whose normal reservoir is a variety of small mammals. Although infection of these natural hosts... (Review)
Review
The spirochete Borrelia burgdorferi is a tick-borne obligate parasite whose normal reservoir is a variety of small mammals. Although infection of these natural hosts does not lead to disease, infection of humans can result in Lyme disease as a consequence of the human immunopathologic response to B burgdorferi. Consistent with the pathogenesis of Lyme disease, bacterial products that allow B burgdorferi to replicate and survive seem to be primarily what is required for the bacterium to cause disease in a susceptible host. This article describes the basic biology of B burgdorferi and reviews some of the bacterial components required for infection of and survival in the mammalian and tick hosts.
Topics: Animals; Arachnid Vectors; Borrelia burgdorferi; Disease Models, Animal; Genome, Bacterial; Humans; Life Cycle Stages; Lyme Disease; Ticks
PubMed: 18452798
DOI: 10.1016/j.idc.2007.12.013 -
Cellular Microbiology Feb 2019Borrelia burgdorferi is the causative agent of Lyme disease that persists in a complex enzootic life cycle, involving Ixodes ticks and vertebrate hosts. The microbe... (Review)
Review
Borrelia burgdorferi is the causative agent of Lyme disease that persists in a complex enzootic life cycle, involving Ixodes ticks and vertebrate hosts. The microbe invades ticks and vertebrate hosts in spite of active immune surveillance and potent microbicidal responses, and establishes long-term infection utilising mechanisms that are yet to be unravelled. The pathogen can cause multi-system disorders when transmitted to susceptible mammalian hosts, including in humans. In the past decades, several studies identified a limited number of B. burgdorferi gene-products critical for pathogen persistence, transmission between the vectors and the host, and host-pathogen interactions. This review will focus on the interactions between B. burgdorferi proteins, as well as between microbial proteins and host components, protein and non-protein components, highlighting their roles in pathogen persistence in the mammalian host. A better understanding of the contributions of protein interactions in the microbial virulence and persistence of B. burgdorferi would support development of novel therapeutics against the infection.
Topics: Animals; Bacterial Proteins; Borrelia burgdorferi; Host-Pathogen Interactions; Humans; Ixodes; Lyme Disease; Protein Binding; Protein Interaction Maps; Virulence; Virulence Factors
PubMed: 29934966
DOI: 10.1111/cmi.12885 -
Microbes and Infection Apr 2006We outline in this review how Borrelia burgdorferi, the causative agent of Lyme disease, moves from the tick to the vertebrate host, and what molecules are potentially... (Review)
Review
We outline in this review how Borrelia burgdorferi, the causative agent of Lyme disease, moves from the tick to the vertebrate host, and what molecules are potentially involved in this challenging commute. The survival strategies utilized by the spirochete during transmission and the initial stages of infection are discussed.
Topics: Animals; Arachnid Vectors; Bacterial Proteins; Borrelia burgdorferi; Gene Expression Regulation, Bacterial; Humans; Ixodes; Lyme Disease
PubMed: 16698304
DOI: 10.1016/j.micinf.2005.12.022 -
Future Microbiology Oct 2017The borrelial resurge demonstrates that Borrelia burgdorferi is a persistent health problem. This spirochete is responsible for a global public health concern called... (Review)
Review
The borrelial resurge demonstrates that Borrelia burgdorferi is a persistent health problem. This spirochete is responsible for a global public health concern called Lyme disease. B. burgdorferi faces diverse environmental conditions of its vector and host during its life cycle. To circumvent the host immune system is a prominent feature of B. burgdorferi. To date, numerous studies have reported on the various mechanisms used by this pathogen to evade the host defense mechanisms. This current review attempts to consolidate this information to describe the immunological and molecular methods used by B. burgdorferi for its survival.
Topics: Antigen-Antibody Complex; Antigenic Variation; Antigens, Bacterial; Bacterial Proteins; Borrelia burgdorferi; Cytokines; Gene Expression Regulation, Bacterial; Gene Transfer, Horizontal; Host-Pathogen Interactions; Immune Evasion; Lyme Disease; Recombination, Genetic; Spirochaetales
PubMed: 28972415
DOI: 10.2217/fmb-2017-0013 -
Clinics in Laboratory Medicine Dec 2015Borrelia burgdorferi is the tick-borne etiologic agent of Lyme disease. The spirochete must negotiate numerous barriers in order to establish a disseminated infection in... (Review)
Review
Borrelia burgdorferi is the tick-borne etiologic agent of Lyme disease. The spirochete must negotiate numerous barriers in order to establish a disseminated infection in a mammalian host. These barriers include migration from the feeding tick midgut to the salivary glands, deposition in skin, manipulation or evasion of the localized host immune response, adhesion to and extravasation through an endothelial barrier, hematogenous dissemination, and establishment of infection in distal tissue sites. Borrelia burgdorferi proteins that mediate many of these processes and the nature of the host response to infection are described.
Topics: Animals; Antigens, Bacterial; Borrelia burgdorferi; Humans; Immune Evasion; Immunity, Innate; Integrins
PubMed: 26593255
DOI: 10.1016/j.cll.2015.07.004 -
FEBS Letters Aug 2020Borreliosis (Lyme disease) is a spirochetal disease caused by the species complex of Borrelia burgdorferi transmitted by Ixodes spp. ticks. Recorded to be the most... (Review)
Review
Borreliosis (Lyme disease) is a spirochetal disease caused by the species complex of Borrelia burgdorferi transmitted by Ixodes spp. ticks. Recorded to be the most common tick-borne disease in the world, the last two decades have seen an increase in disease incidence and distribution, exceeding 360 000 cases in Europe alone. If untreated, infection may cause skin symptoms, arthritis, and neurological or cardiac complications. Borrelia spirochetes have developed strategies to evade the mammalian host immune system. These include the complement system, which is an important first-line defense mechanism against invading microbes. To evade the complement, spirochetes bind soluble complement regulators factor H (FH), factor H-like protein, and C4bp to their outer surfaces. B. burgdorferi spirochetes can inhibit the classical pathway of complement by the outer surface protein (Osp) BBK32, which blocks the activation of the C1 complex, composed of C1q, C1r, and C1s. The FH-binding proteins of borreliae include Osps OspE, CspA, and CspZ. Following repeated infections, antibodies against these proteins develop and may provide functional immunity against borreliosis. This review discusses critical immune evasion strategies, focusing on complement evasion by borreliae.
Topics: Animals; Antibodies, Bacterial; Bacterial Proteins; Borrelia burgdorferi; Complement System Proteins; Humans; Immune Evasion; Lyme Disease
PubMed: 32748966
DOI: 10.1002/1873-3468.13894 -
Infection Feb 2011
Topics: Bacteremia; Borrelia burgdorferi; Humans; Lyme Disease
PubMed: 21311945
DOI: 10.1007/s15010-011-0089-5 -
Current Opinion in Microbiology Aug 2023The Lyme disease spirochete persists in nature through cycles between ticks and vertebrates. Although the spirochete interacts with numerous, distinct tissues and... (Review)
Review
The Lyme disease spirochete persists in nature through cycles between ticks and vertebrates. Although the spirochete interacts with numerous, distinct tissues and environmental conditions during its infectious cycle, Borrelia burgdorferi appears to possess a limited ability to sense its external environment. This apparent paradox is being resolved through detailed investigations of the molecular mechanisms through which B. burgdorferi controls production of virulence-associated factors such as the Erp outer surface proteins. The results have led to development of a model for how B. burgdorferi controls expression of its diverse proteins, wherein physiological and metabolic states that are unique to specific points in the infectious cycle trigger changes in gene and protein expression levels.
Topics: Animals; Borrelia burgdorferi; Bacterial Proteins; Ticks; Lyme Disease
PubMed: 37279610
DOI: 10.1016/j.mib.2023.102332 -
Current Topics in Microbiology and... 2017The spirochete Borrelia burgdorferi is the causative agent of Lyme disease, a multisystemic disorder affecting primarily skin, nervous system, and joints. If an... (Review)
Review
The spirochete Borrelia burgdorferi is the causative agent of Lyme disease, a multisystemic disorder affecting primarily skin, nervous system, and joints. If an infection with Borrelia proceeds unchecked, the disease can also enter a chronic stage, leading to the development of neuroborreliosis or cardiac arrhythmia. Successful elimination of B. burgdorferi by the host immune system is thus decisive for the positive outcome of a respective infection. Accordingly, host immune cells such as macrophages and dendritic cells have to be able to efficiently internalize and degrade infecting spirochetes. These processes are based on closely controlled rearrangements of the actin cytoskeleton, which enables the spatiotemporally fine-tuned formation of cellular protrusions and compartments that assist in the capturing, immobilization, and uptake of borreliae, as well as their further intracellular processing. Here, we discuss actin-based structures, in particular filopodia and coiling pseudopods that are involved in phagocytosis of B. burgdorferi by macrophages, their regulation by actin-associated proteins such as formins and Arp2/3 complex, as well as the subsequent intracellular processing of borreliae.
Topics: Actins; Animals; Borrelia burgdorferi; Humans; Lyme Disease; Macrophages; Phagocytosis
PubMed: 27744511
DOI: 10.1007/82_2016_26 -
Frontiers in Cellular and Infection... 2014Lyme disease is a long-term infection whose most severe pathology is characterized by inflammatory arthritis of the lower bearing joints, carditis, and neuropathy. The... (Review)
Review
Lyme disease is a long-term infection whose most severe pathology is characterized by inflammatory arthritis of the lower bearing joints, carditis, and neuropathy. The inflammatory cascades are initiated through the early recognition of invading Borrelia burgdorferi spirochetes by cells of the innate immune response, such as neutrophils and macrophage. B. burgdorferi does not have an intracellular niche and thus much research has focused on immune pathways activated by pathogen recognition molecules at the cell surface, such as the Toll-like receptors (TLRs). However, in recent years, studies have shown that internalization of the bacterium by host cells is an important component of the defense machinery in response to B. burgdorferi. Upon internalization, B. burgdorferi is trafficked through an endo/lysosomal pathway resulting in the activation of a number of intracellular pathogen recognition receptors including TLRs and Nod-like receptors (NLRs). Here we will review the innate immune molecules that participate in both cell surface and intracellular immune activation by B. burgdorferi.
Topics: Animals; Borrelia burgdorferi; Host-Pathogen Interactions; Humans; Immunity, Innate; Lyme Disease
PubMed: 25566512
DOI: 10.3389/fcimb.2014.00175