OspB Antibody Prevents
            <i>Borrelia burgdorferi</i>
            Colonization of
            <i>Ixodes scapularis</i>

Fikrig, Erol; Pal, Utpal; Chen, Manchuan; Anderson, John F.; Flavell, Richard A.

doi:10.1128/iai.72.3.1755-1759.2004

Cited by 39 publications

(39 citation statements)

References 23 publications

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“…Host cell-specific differential protein expression in vertebrate and tick cells, including those from the p28-Omp multigene locus encoding outer membrane antigens, may be one of the mechanisms that aid the persistence of E. chaffeensis in tick and vertebrate hosts. Differential gene expression by B. burgdorferi, a tick-transmitted spirochete, within a host has been demonstrated and appears to contribute to its adaptation in dual hosts (12,15,44). B. burgdorferi expresses outer surface protein A (OspA) when it enters its tick host, Ixodes scapularis, and continues to produce abundant OspA within the resting tick (references in reference 12).…”

Section: Vol 73 2005mentioning

confidence: 99%

“…Understanding the molecular events of bacterial adaptation to tick and vertebrate hosts will be valuable for the development of effective control strategies. Recent studies on B. burgdorferi suggest that the pathogen's adaptation involves the expression of unique hostspecific surface antigens (12,15,44). Recent studies on Anaplasma species also suggest the differential expression of surface proteins in tick and mammalian hosts (22,25,43).…”

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confidence: 99%

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Ehrlichia chaffeensis Expresses Macrophage- and Tick Cell-Specific 28-Kilodalton Outer Membrane Proteins

et al. 2005

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Ehrlichia chaffeensis, a tick-transmitted rickettsial agent, causes human monocyte/macrophage-tropic ehrlichiosis. In this study, proteomic approaches were used to demonstrate host cell-specific antigenic expression by E. chaffeensis. The differentially expressed antigens include those from the 28-kDa outer membrane protein (p28-Omp) multigene locus. The proteins expressed in infected macrophages are the products of p28-Omp19 and p28-Omp20 genes, whereas in tick cells, the protein expressed is the p28-Omp14 gene product. The differentially expressed proteins are posttranslationally modified by phosphorylation and glycosylation to generate multiple expressed forms. Host cell-specific protein expression is not influenced by growth temperatures and is reversible. Host cell-specific protein expression coupled with posttranslational modifications may be a hallmark for the pathogen's adaptation to a dual-host life cycle and its persistence.

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Section: Vol 73 2005mentioning

confidence: 99%

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confidence: 99%

Ehrlichia chaffeensis Expresses Macrophage- and Tick Cell-Specific 28-Kilodalton Outer Membrane Proteins

et al. 2005

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“…Recombinant OspD was further purified on a Superdex 200 column (Amersham Biosciences) and used to immunize mice to generate antisera. Recombinant OspA, OspB, OspC, and Dps proteins (6,12,20) were also expressed as GST fusions with the expression vector pGEX6p2 (Amersham Biosciences). Similarly, the GST tag was removed from the recombinant proteins during purification as described above.…”

Section: Pcr and Quantitative Pcr (Q-pcr)mentioning

confidence: 99%

Role of Outer Surface Protein D in theBorrelia burgdorferiLife Cycle

Neelakanta

Liu

et al. 2007

Infect Immun

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Borrelia burgdorferi preferentially induces selected genes in mice or ticks, and studies suggest that ospD is down-regulated in response to host-specific signals. We now directly show that ospD expression is generally elevated within Ixodes scapularis compared with mice. We then assessed the importance of OspD throughout the spirochete life cycle by generating OspD-deficient B. burgdorferi and examining the mutant in the murine model of tick-transmitted Lyme borreliosis. The lack of OspD did not influence B. burgdorferi infectivity in mice or the acquisition of spirochetes by I. scapularis. OspD adhered to tick gut extracts in vitro, and the OspD-deficient B. burgdorferi strain had a threefold decrease in colonization of the tick gut in vivo. This decrease, however, did not alter subsequent spirochete transmission during a second blood meal. These data suggest that B. burgdorferi can compensate for the lack of OspD in both ticks and mice and that OspD may have a nonessential, secondary, role in B. burgdorferi persistence within I. scapularis.

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“…Moreover, B. burgdorferi OspA gene expression may allow adhesion to the midgut, but the expression of OspC genes may allow the invasion of tick salivary glands as a prerequisite to vertebrate host infection (22). Therefore, differential antigen expression may facilitate movement between the arthropods and mammals for tick-transmitted bacteria (14,21,41,45).…”

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confidence: 99%

Differential Clearance and Immune Responses to Tick Cell-Derived versus Macrophage Culture-DerivedEhrlichia chaffeensisin Mice

Ganta¹,

Cheng²,

Miller

et al. 2007

Infect Immun

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Human monocytic ehrlichiosis is caused by a tick-transmitted rickettsia, Ehrlichia chaffeensis. We recently reported that E. chaffeensis grown in tick cells expresses different proteins than bacteria grown in macrophages. Therefore, we tested the hypothesis that immune responses against E. chaffeensis would be different if the mice are challenged with bacteria grown in macrophages or tick cells. We assessed the E. chaffeensis clearance from the peritoneum, spleen, and liver by C57BL/6J mice using a TaqMan-based real-time reverse transcription-PCR assay. Macrophage-grown E. chaffeensis was cleared in 2 weeks from the peritoneum, whereas the pathogen from tick cells persisted for nine additional days and included three relapses of increasing bacterial load separated by three-day intervals. Tick cell-grown bacteria also persisted in the livers and spleens with higher bacterial loads compared to macrophage-grown bacteria and fluctuated over a period of 35 days. Three-day periodic cycles were detected in T-cell CD62L/CD44 ratios in the spleen and bone marrow in response to infections with both tick cell-and macrophage-grown bacteria and were accompanied by similar periodic cycles of spleen cell cytokine secretions and nitric oxide and interleukin-6 by peritoneal macrophages. The E. chaffeensis-specific immunoglobulin G response was considerably higher and steadily increased in mice infected with the tick cell-derived E. chaffeensis compared to DH82-grown bacteria. In addition, antigens detected by the immunoglobulins were significantly different between mice infected with the E. chaffeensis originating from tick cells or macrophages. The differences in the immune response to tick cell-grown bacteria compared to macrophage-grown bacteria reflected a delay in the shift of gene expression from the tick cell-specific Omp 14 gene to the macrophage-specific Omp 19 gene. These data suggest that the host response to E. chaffeensis depends on the source of the bacteria and that this experimental model requires the most natural inoculum possible to allow for a realistic understanding of host resistance.

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OspB Antibody Prevents Borrelia burgdorferi Colonization of Ixodes scapularis

Cited by 39 publications

References 23 publications

Ehrlichia chaffeensis Expresses Macrophage- and Tick Cell-Specific 28-Kilodalton Outer Membrane Proteins

Ehrlichia chaffeensis Expresses Macrophage- and Tick Cell-Specific 28-Kilodalton Outer Membrane Proteins

Role of Outer Surface Protein D in theBorrelia burgdorferiLife Cycle

Differential Clearance and Immune Responses to Tick Cell-Derived versus Macrophage Culture-DerivedEhrlichia chaffeensisin Mice

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