Intracellular persistence ofBorrelia burgdorferi in human synovial cells

Girschick, H. J.; Huppertz, HI; Rüssmann, Holger; Krenn, Veit; Karch, Helge

doi:10.1007/bf01409985

Cited by 124 publications

(91 citation statements)

References 30 publications

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“…It has been postulated that borrelia interacts with the complement, inactivating complement regulatory proteins (Kraiczy et al, 2001(Kraiczy et al, , 2002. Others have proved that Bb can hide in immunoprivileged sites (de Koning et al, 1995;Girschick et al, 1996). The antigen variation of the Bb outer membrane has also been discussed as a possible strategy for evading the immune response (Seiler and Weis, 1996;Zhang et al, 1997).…”

Section: Discussionmentioning

confidence: 99%

Mycosis fungoides: is it a Borrelia burgdorferi-associated disease?

et al. 2006

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Mycosis fungoides (MF) is the most frequently found cutaneous T-cell lymphoma with an unknown aetiology. Several aetiopathogenetic mechanisms have been postulated, including persistent viral or bacterial infections. We looked for evidence of Borrelia burgdorferi (Bb), the aetiologic agent of Lyme disease (LD), in a case study of MF patients from Northeastern Italy, an area with endemic LD. Polymerase chain reaction for the flagellin gene of Bb was used to study formalin-fixed paraffin-embedded lesional skin biopsies from 83 patients with MF and 83 sex-and age-matched healthy controls with homolocalised cutaneous nevi. Borrelia burgdorferi-specific sequence was detected in 15 out of 83 skin samples of patients with MF (18.1%), but in none out of 83 matched healthy controls (Po0.0001). The Bb positivity rates detected in this study support a possible role for Bb in the aetiopathogenesis of MF in a population endemic for LD.

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Section: Discussionmentioning

confidence: 99%

Mycosis fungoides: is it a Borrelia burgdorferi-associated disease?

et al. 2006

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“…Although a number of putative mechanisms for their immune evasion have been described, such as antigenic variation (51), binding of host-derived enzymes (52-54), or intracellular survival (55,56), it is presently unclear if any of these strategies contribute to the persistence of spirochetes. Our finding that chronic B. burgdorferi infection of SCID mice is resolved by Abs to OspC, at least for Ͼ80 days p.i., strongly indicates that in vivo the majority of spirochetes are localized extracellularly in affected tissues of the mammalian host.…”

Section: Discussionmentioning

confidence: 99%

Therapeutic passive vaccination against chronic Lyme disease in mice

Zhong

Stehlé

Museteanu

et al. 1997

Proc. Natl. Acad. Sci. U.S.A.

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Passive and active immunization against outer surface protein A (OspA) has been successful in protecting laboratory animals against subsequent infection with Borrelia burgdorferi. Antibodies (Abs) to OspA convey full protection, but only when they are present at the time of infection. Abs inactivate spirochetes within the tick and block their transmission to mammals, but do not affect established infection because of the loss of OspA in the vertebrate host. Our initial finding that the presence of high serum titers of anti-OspC Abs (5 to 10 g͞ml) correlates with spontaneous resolution of disease and infection in experimentally challenged immunocompetent mice suggested that therapeutic vaccination with OspC may be feasible. We now show that polyclonal and monospecific mouse immune sera to recombinant OspC, but not to OspA, of B. burgdorferi resolve chronic arthritis and carditis and clear disseminated spirochetes in experimentally infected C.B.-17 severe combined immunodeficient mice in a dose-dependent manner. This was verified by macroscopical and microscopical examination of affected tissues and recultivation of spirochetes from ear biopsies. Complete resolution of disease and infection was achieved, independent of whether OspC-specific immune sera (10 g OspC-specific Abs) were repeatedly given (4؋ in 3-to 4-day intervals) before the onset (day 10 postinfection) or at the time of fully established arthritis and carditis (days 19 or 60 postinfection). The results indicate that in mice spirochetes constitutively express OspC and are readily susceptible to protective OspC-specific Abs throughout the infection. Thus, an OspC-based vaccine appears to be a candidate for therapy of Lyme disease.

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“…It is still unclear how Borrelia infection can persist in an immunocompetent host. Several hypothesis have been put forward: (i) localization of the spirochetes in immunoprivileged sites such as intracellular compartments (11), as well as in the extracellular matrix (18), as a rationale for how the pathogen escapes the immune system; (ii) a high variation of surface antigens in B. burgdorferi (31), similar to Borrelia hermsii, which causes relapsing fever (30); this surface antigen modulation could explain how Borrelia evades the immune response; (iii) a shift in the T-helper-cell response as the cause of the treatment-resistant form of Lyme disease (22); (iv) a self-propagating induction of autoimmunity following infection with Borrelia to become a chronic disease, recently supported by the finding that the Borrelia outer surface protein A (OspA) is homologous to the human LFA-1 antigen (12); and (v) modulation of the host immune response by the pathogen in a way that enables survival of the pathogen.…”

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confidence: 99%